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1.
  • Scherstén, Henrik, 1956, et al. (author)
  • ECMO kan vara brygga till lungtransplantation : Ny metod räddar liv vid akut lungsvikt, visar retrospektiv studie.
  • 2011
  • In: Läkartidningen. - 0023-7205. ; 108:32-33, s. 1493-7
  • Journal article (peer-reviewed)abstract
    • Lungtransplantation har utförts i Sverige sedan 20 år. Patienter som snabbt försämras i akut lungsvikt och inte återhämtar sig med konservativ behandling har tidigare bedömts som inte transplantabla och därför avlidit. Sedan några år använder vi i utvalda fall extrakorporeal membranoxygenering (ECMO) som brygga till lungtransplantation hos annars döende patienter. Överlevnaden för patienter som behandlats med ECMO syftande till lungtransplantation var 73 procent (8/11). Överlevnaden för dem som sedan genomgick lungtransplantation var 89 procent (8/9). Ingreppen genererade en hel del morbiditet, dock mest av övergående natur. Vi anser att ECMO-behandling i selekterade fall kan erbjudas yngre och medelålders patienter, trots att behandlingen i sig väcker frågor om morbiditet, kostnader och resursförbrukning. Det återstår att utvärdera långtidsresultaten hos patienter som genomgått ECMO-behandling som brygga till lungtransplantation.
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2.
  • Scherstén, Henrik, 1956, et al. (author)
  • Increased levels of endothelin-1 in bronchoalveolar lavage fluid of patients with lung allografts
  • 1996
  • In: J Thorac Cardiovasc Surg. - 0022-5223. ; 111:1, s. 253-8
  • Journal article (peer-reviewed)abstract
    • The aim of the present study was to determine levels of endothelin-1 in bronchoalveolar lavage fluid and in plasma in patients with lung and heart-lung allografts. The aim was based on the hypothesis that levels of endothelin-1 are elevated in the bronchoalveolar lavage fluid of patients with lung allografts. Patients (n = 23) undergoing heart-lung (n = 8), single-lung (n = 10), or bilateral lung (n = 5) transplantation were included in the study. In patients with single-lung allografts, endothelin-1 levels were analyzed in bronchoalveolar lavage fluid from both the transplanted and the nontransplanted, native lung. The level of endothelin-1 was also analyzed in bronchoalveolar lavage fluid from 12 patients who did not undergo transplantation. Transbronchial biopsies and bronchoalveolar lavage were done routinely or when clinically indicated on 64 different occasions, between 2 and 104 weeks after transplantation. The level of endothelin-1 was measured in bronchoalveolar lavage fluid and plasma by radioimmunoassay. Immunoreactive endothelin-1 was detectable in bronchoalveolar lavage fluid from all patients. The concentration of endothelin-1 in bronchoalveolar lavage fluid from transplanted lungs (2.94 +/- 0.30 pg/ml, n = 64) was significantly higher compared with that in bronchoalveolar lavage fluid from patients without allografts (0.86 +/- 0.20 pg/ml, n = 12, p < 0.01). In patients who received single-lung transplantation because of emphysema, the level of endothelin-1 in bronchoalveolar lavage fluid from the transplanted lung was significantly greater than that from the native lung (5.61 +/- 1.9 versus 0.39 +/- 0.05 pg/ml, p < 0.05). Concentrations of endothelin-1 in bronchoalveolar lavage fluid did not correlate with grade of rejection, infection, or time after transplant. Plasma levels of endothelin-1 were unchanged with pulmonary rejection. These results indicate that endothelin-1 is released into bronchi of transplanted human lungs. The release is not associated with rejection or infection. Because of its potent mitogenic properties, endothelin-1 may have a potential impact in the development of posttransplant complications such as bronchiolitis obliterans.
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3.
  • Baker, N, et al. (author)
  • Glycosphingolipid receptors for Pseudomonas aeruginosa.
  • 1990
  • In: Infection and immunity. - 0019-9567. ; 58:7, s. 2361-6
  • Journal article (peer-reviewed)abstract
    • The binding of Pseudomonas aeruginosa to glycosphingolipids and to buccal and bronchial epithelial cells was analyzed. Three independently expressed specificities were found by bacterial binding to glycosphingolipids separated by thin-layer chromatography. All strains bound gangliotria- and gangliotetrasylceramide. All but one of the strains bound sialic acid-containing glycosphingolipids and lactosylceramide. The latter two specificities could be separated in that the lactosylceramide binding was retained and the sialic acid binding was suppressed when bovine serum albumin was used as a blocking agent in the thin-layer chromatography assay. The attachment to buccal epithelial cells, like the binding to sialylated compounds and lactosylceramide, was abolished by Formalin treatment of the bacteria, suggesting the importance of these specificities for cell adherence. In contrast, the binding to gangliotria- and gangliotetraosylceramide was retained by nonattaching Formalin-treated bacteria.
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6.
  • Mattsson Hultén, Lillemor, 1951, et al. (author)
  • Butylated hydroxytoluene and N-acetylcysteine attenuates tumor necrosis factor-alpha (TNF-alpha) secretion and TNF-alpha mRNA expression in alveolar macrophages from human lung transplant recipients in vitro
  • 1998
  • In: Transplantation. - 0041-1337. ; 66:3, s. 364-9
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a polypeptide cytokine principally produced by macrophages/monocytes and commonly associated with inflammatory conditions. The present study was designed to investigate whether the antioxidants butylated hydroxytoluene (BHT) and N-acetylcysteine (NAC) modified TNF-alpha production in stimulated and unstimulated alveolar macrophages from lung transplant recipients in vitro. METHODS: The effects of BHT and NAC on TNF-alpha production were studied both with and without lipopolysaccharide (LPS) activation of alveolar macrophages from bronchoalveolar lavage fluid. TNF-alpha was quantitated in cell culture medium using an enzyme-linked immunosorbent assay. TNF-alpha mRNA expression was analyzed by quantitative reverse transcription-polymerase chain reaction on total RNA extracted from the incubated alveolar macrophages. RESULTS: In unstimulated alveolar macrophages, TNF-alpha levels were significantly reduced by incubation with BHT or NAC. When alveolar macrophages from patients with cytomegalovirus infection were incubated with BHT, TNF-alpha secretion was significantly lowered. A significant reduction of TNF-alpha levels in LPS-stimulated alveolar macrophages was obtained in the presence of BHT or NAC. Our data from quantitative reverse transcription-polymerase chain reaction showed that the observed decrease in protein levels of TNF-alpha was associated with a decrease in TNF-alpha mRNA expression. CONCLUSIONS: Our results indicate that antioxidant treatment may be an effective step to lower the inflammatory process caused by cytomegalovirus infection or in endotoxin (LPS)-activated macrophages. The therapeutic use of antioxidant compounds could, therefore, be of interest in conditions such as lung transplantation, in which oxidative stress and inflammation can contribute significantly to the loss of allograft function.
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7.
  • Nordén, Rickard, 1977, et al. (author)
  • Quantification of torque teno virus and Epstein-Barr virus is of limited value for predicting the net state of immunosuppression after lung transplantation
  • 2018
  • In: Open Forum Infectious Diseases. - : Oxford University Press (OUP). - 2328-8957. ; 5:4
  • Journal article (peer-reviewed)abstract
    • Background. Major hurdles for survival after lung transplantation are rejections and infectious complications. Adequate methods for monitoring immune suppression status are lacking. Here, we evaluated quantification of torque teno virus (TTV) and Epstein-Barr virus (EBV) as biomarkers for defining the net state of immunosuppression in lung-transplanted patients. Methods. This prospective single-center study included 98 patients followed for 2 years after transplantation. Bacterial infections, fungal infections, viral respiratory infections (VRTI), cytomegalovirus (CMV) viremia, and acute rejections, as well as TTV and EBV levels, were monitored. Results. The levels of torque teno virus DNA increased rapidly after transplantation, likely due to immunosuppressive treatment. A modest increase in levels of Epstein-Barr virus DNA was also observed after transplantation. There were no associations between either TTV or EBV and infectious events or acute rejection, respectively, during follow-up. When Tacrolimus was the main immunosuppressive treatment, TTV DNA levels were significantly elevated 6-24 months after transplantation as compared with Cyclosporine treatment. Conclusions. Although replication of TTV, but not EBV, appears to reflect the functionality of the immune system, depending on the type of immunosuppressive treatment, quantification of TTV or EBV as biomarkers has limited potential for defining the net state of immune suppression.
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8.
  • Riise, Gerdt C., 1956, et al. (author)
  • Activation of eosinophils and fibroblasts assessed by eosinophil cationic protein and hyaluronan in BAL. Association with acute rejection in lung transplant recipients
  • 1996
  • In: Chest. - 0012-3692. ; 110:1, s. 89-96
  • Journal article (peer-reviewed)abstract
    • Lung transplantation has become an accepted therapy for end-stage lung disease. Acute rejection of the transplanted hung still remains a major clinical problem since it decreases graft survival. Eosinophil cationic protein (ECP) from activated eosinophils, hyaluronan (HYA) from fibroblasts, and circulating intercellular adhesion molecule 1 (1CAM-1) have been associated with acute rejection in kidney and liver grafts. We investigated whether these, as well as other molecules, were increased in acute rejection of lung allografts. Serum and BAL fluid from 38 bronchoscopies performed in 9 single lung, 2 bilateral lung, and 4 heart-lung transplant patients were studied. Differential cell counts were made from the BAL fluid. Levels of ECP, myeloperoxidase (MPO), and HYA were used as indirect markers for activation of eosinophils, neutrophils, and fibroblasts, respectively. In addition, levels of circulating ICAM-1, cVCAM-1, and cE-selectin were analyzed. Twenty-two episodes with acute rejection were diagnosed. Of these, 7 were minimal, 13 were mild, and 2 were of moderate character. We found increased levels of ECP and HYA in BAL fluid during mild acute rejection of the allograft. Numbers of eosinophils were also increased. Activation of neutrophils or neutrophil numbers were not significantly increased. Levels of circulating ICAM-1, cVCAM-1, and cE-selectin did not differ between the groups. This retrospective study shows that measurements of ECP and HYA can give information about the inflammatory process present during acute rejection in patients who have undergone lung transplants. Analysis of cCAMS, however, appears to be of limited value as markers for acute rejection.
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9.
  • Riise, Gerdt C., 1956, et al. (author)
  • Bronchiolitis obliterans syndrome in lung transplant recipients is associated with increased neutrophil activity and decreased antioxidant status in the lung
  • 1998
  • In: Eur Respir J. - 0903-1936. ; 12:1, s. 82-8
  • Journal article (peer-reviewed)abstract
    • Long-term survival of lung transplant recipients is limited by the advent of obliterative bronchiolitis and irreversible airways obstruction, e.g. bronchiolitis obliterans syndrome (BOS). This study investigated whether inflammatory cells and their activation markers were increased in bronchoalveolar lavage (BAL) and transbronchial biopsies (TBB) from patients with BOS. Levels of antioxidants in BAL fluid were also assessed. BAL fluid and TBB from six single-lung, two bilateral-lung, and five heart-lung transplanted patients with diagnosis of BOS were compared with 13 transplant recipients without BOS. BAL fluid levels of myeloperoxidase (MPO), eosinophil cationic protein (ECP) and interleukin (IL)-8 were used as markers for the activation and attraction of neutrophils and eosinophils, respectively. Immunohistochemical staining of TBB with monoclonal antibodies to MPO and ECP (EG2) was performed. Significantly increased BAL percentages of neutrophils and levels of MPO were found in patients with BOS. The findings correlated well with the degree of monoclonal staining for MPO in TBB. BAL levels of ECP and IL-8 were significantly increased in BOS patients. BAL concentrations of the water-soluble antioxidants ascorbate, urate and glutathione were generally lower in BOS patients. The results indicate that neutrophil infiltration and activation, as well as oxidative stress, may play a role in the development and/or progression of bronchiolitis obliterans syndrome. Markers for neutrophil activation could have a potential role in monitoring disease activity in patients with this syndrome.
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10.
  • Riise, Gerdt C., 1956, et al. (author)
  • Inflammatory cells and activation markers in BAL during acute rejection and infection in lung transplant recipients: a prospective, longitudinal study
  • 1997
  • In: Eur Respir J. - 0903-1936. ; 10:8, s. 1742-6
  • Journal article (peer-reviewed)abstract
    • Acute rejection of the transplanted lung is a clinical problem, since it decreases graft survival and predisposes the patient to chronic rejection and obliterative bronchiolitis (OB). In an earlier study, we had indications that eosinophil cationic protein (ECP) from activated eosinophils and hyaluronan (HYA) from fibroblasts were associated with acute pulmonary rejection. This prospective longitudinal study was designed to investigate whether molecules from activated inflammatory cells in bronchoalveolar lavage (BAL) fluid could serve as clinically useful diagnostic markers for acute rejection. BAL fluid from 138 bronchoscopies performed in 10 single lung, four bilateral lung and five heart-lung transplant recipients were analysed. Nine patients were studied for a period of more than 1 yr (mean 13.4 months) after surgery. Differential cell counts were made from the BAL fluid. ECP, myeloperoxidase (MPO), HYA and interleukin-8 (IL-8) were used as indirect markers for activation and attraction of eosinophils, neutrophils and fibroblasts, respectively. Fifty four episodes of acute rejection were diagnosed. Two patients developed OB. Nine episodes of bacterial infection, 13 episodes of cytomegalovirus (CMV) pneumonitis, three of Pneumocystis carinii infection and one of respiratory syncytial virus (RSV) infection were diagnosed. The mean levels of ECP, MPO, HYA and IL-8 were all higher during rejection episodes, but differences were not statistically significant compared to no rejection, when the confounding factors of time, concomitant infection, and repeated measures in the same individual had been accounted for. We could not confirm that measurements of eosinophil cationic protein, myeloperoxidase, hyaluronan and interleukin-8 in bronchoalveolar lavage fluid can be used as diagnostic markers for acute rejection in the postoperative follow-up of lung transplant recipients.
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11.
  • Riise, Gerdt C., 1956, et al. (author)
  • Persistent high BAL fluid granulocyte activation marker levels as early indicators of bronchiolitis obliterans after lung transplant
  • 1999
  • In: Eur Respir J. - 0903-1936. ; 14:5, s. 1123-30
  • Journal article (peer-reviewed)abstract
    • The major cause of mortality in the long-term in lung transplant recipients is chronic rejection. This is a fibroproliferative process in the small airways leading to obliterative bronchiolitis and progressive loss of lung function, both constituting the clinical entity bronchiolitis obliterans syndrome (BOS). Granulocyte activation has been implicated as one factor behind BOS. Granulocyte markers in bronchoalveolar lavage (BAL) fluid were prospectively and longitudinally studied in order to identify possible association with BOS. BAL fluid from 266 bronchoscopy procedures performed in twelve single lung, eight bilateral lung and five heart/lung transplant recipients were analysed. The majority (19 of 25) were studied for a period of 2 yrs after surgery. Myeloperoxidase (MPO), eosinophil cationic protein (ECP) and interleukin-8 (IL-8) levels were used as indirect markers of activation and attraction of granulocytes. Five patients developed BOS. Ninety-eight episodes of acute rejection, nine of bacterial infection, 19 of cytomegalovirus pneumonitis, nine of Pneumocystis carinii infection, two of aspergillus infection and two of respiratory syncytial virus infection were diagnosed. BOS patients had significantly higher mean levels of MPO, ECP and IL-8 compared to patients without BOS, irrespective of acute rejection status. Over time, the five patients with BOS had significantly elevated BAL fluid levels of MPO and ECP as well as neutrophil percentages, and in four patients this increase preceded the clinical diagnosis of BOS by several months. Elevated bronchoalveolar lavage fluid neutrophil percentage as well as levels of the granulocyte activation markers myeloperoxidase and eosinophil cationic protein appear to be early signs of development of BOS in lung transplant recipients.
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12.
  • Wagner, C. S., et al. (author)
  • Increased expression of leukocyte Ig-like receptor-1 and activating role of UL18 in the response to cytomegalovirus infection
  • 2007
  • In: J Immunol. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 178:6, s. 3536-43
  • Journal article (peer-reviewed)abstract
    • NK and T cells are important for combating CMV infection. Some NK and T cells express leukocyte Ig-like receptor-1 (LIR-1), an inhibitory receptor recognizing MHC class I and the CMV-encoded homolog UL18. We previously demonstrated an early increase in LIR-1-expressing blood lymphocytes in lung-transplanted patients later developing CMV disease. We now show that NK and T cells account for the observed LIR-1 augmentation. Coincubation of PBMC from CMV-seropositive donors with virus-infected lung fibroblasts led to a T cell-dependent secretion of IFN-gamma, produced mainly by LIR-1(+) T cells and by NK cells. Cytokine production during coculture with fibroblasts infected with virus containing the UL18 gene was augmented compared with the UL18 deletion virus, suggesting a stimulatory role for UL18. However, purified UL18Fc proteins inhibited IFN-gamma production of LIR-1(+) T cells. We propose that cytokine production in the transplant induces NK and T cells to express LIR-1, which may predispose to CMV disease by MHC/LIR-1-mediated suppression. Although the UL18/LIR-1 interaction could inhibit T cell responses, this unlikely plays a role in response to infected cells. Instead, our data point to an activating role for viral UL18 during infection, where indirect intracellular effects cannot be excluded.
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13.
  • Wallinder, Andreas, 1977, et al. (author)
  • Transplantation of initially rejected donor lungs after exvivo lung perfusion.
  • 2012
  • In: The Journal of thoracic and cardiovascular surgery. - : Elsevier BV. - 1097-685X .- 0022-5223. ; 144:5, s. 1222-1228
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: Exvivo lung perfusion has the potential to increase the number of patients treated with lung transplantation. Our initial clinical experience with exvivo lung perfusion is reviewed as well as early clinical outcome in patients transplanted with reconditioned lungs. METHODS: Six pairs of donor lungs deemed unsuitable for transplantation underwent exvivo lung perfusion with Steen solution mixed with red blood cells to a hematocrit of 10% to 15%. After reconditioning, lung function was evaluated and acceptable lungs were transplanted. Technical experience with exvivo lung perfusion as well as clinical outcome for patients transplanted with exvivo lung perfusion-treated lungs were evaluated. RESULTS: Donor lungs initially rejected either as a result of an inferior partial pressure of arterial oxygen/ fraction of inspired oxygen (n=5; mean, 20.5 kPa; range, 9.1-29.9 kPa) or infiltrate on chest radiograph (n=1) improved their oxygenation capacity to a mean partial pressure of arterial oxygen/fraction of inspired oxygen of 57 ± 10 kPa during the exvivo lung perfusion (mean improvement, 33.6 kPa; range, 21-51 kPa; P<.01). During evaluation, hemodynamic (flow, vascular resistance, pressure) and respiratory (peak airway pressure, compliance) parameters were stable. Two single lungs were not used for lung transplantation because of subpleural hematoma or edema. Six recipients from the regular waiting list underwent single (n=2) or double (n=4) lung transplantation. One patient had primary graft dysfunction grade 2 at 72 hours. Median time to extubation was 7 hours. All patients survived 30 days and were discharged in good condition from the hospital. CONCLUSIONS: The use of ex vivo lung perfusion seems safe and indicates that some lungs otherwise refused for lung transplantation can be recovered and transplanted with acceptable short-term results.
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14.
  • Williams, A., et al. (author)
  • Compromised antioxidant status and persistent oxidative stress in lung transplant recipients
  • 1999
  • In: Free Radic Res. - 1071-5762. ; 30:5, s. 383-93
  • Journal article (peer-reviewed)abstract
    • Oxidative stress may be a key feature, and hence important determinant, of tissue injury and allograft rejection in lung transplant recipients. To investigate this, we determined the antioxidant status (urate, ascorbate, thiols and alpha-tocopherol) and lipid peroxidation status (malondialdehyde) in bronchoalveolar lavage (BAL) fluid and blood serum of 19 consecutive lung transplant recipients 2 weeks and 1, 2, 3, 6, and 12 months post-surgery. BAL fluid and blood samples from 23 control subjects and blood from 8 patients two days before transplantation were obtained for comparison. Before surgery, the antioxidant status of patients was poor as serum ascorbate and total thiol concentrations were significantly (p < 0.05) lower than control subjects. Two weeks post-surgery, ascorbate and total thiol concentrations were still low and urate concentrations had fallen compared to control subjects (p < 0.01). At this time, BAL fluid urate concentration was higher (p < 0.01), ascorbate concentration was lower (p < 0.01) and reduced glutathione concentrations were similar to control subjects. MDA, a product of lipid peroxidation, was higher (p < 0.01) in both BAL fluid and serum obtained from transplant patients compared to control subjects. During the first 12 months post-surgery, little improvement in antioxidant status or extent of lipid peroxidation was seen in transplant recipients. Regression analysis indicated no difference in serum or BAL fluid antioxidant status in patients with acute rejection compared to those without. In conclusion, lung transplant recipients have a compromised antioxidant status before surgery and it remains poor for at least the first year following the operation. In addition, these patients have elevated MDA concentrations in both their lung lining fluid and blood over most of this time. Oxidative stress is not, however, a sufficiently sensitive endpoint to predict tissue rejection in this group.
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15.
  • Andersson, Anders, et al. (author)
  • Effects of Tobacco Smoke on IL-16 in CD8+ Cells from Human Airways and Blood: a Key Role for Oxygen Free Radicals?
  • 2011
  • In: AJP - Lung cellular and molecular physiology. - : American Physiological Society. - 1522-1504. ; 300:1
  • Journal article (peer-reviewed)abstract
    • Chronic exposure to tobacco smoke leads to an increase in the frequency of infections and in CD8(+) and CD4(+)cells as well as the CD4(+) chemo-attractant cytokine IL-16 in the airways. Here, we investigated whether tobacco smoke depletes intracellular IL-16 protein and inhibits de novo production of IL-16 in CD8(+) cells from human airways and blood, while at the same time increasing extracellular IL-16 and whether oxygen free radicals (OFR) are involved. Intracellular IL-16 protein in CD8(+) cells and mRNA in all cells was decreased in bronchoalveolar lavage (BAL) samples from chronic smokers. This was also the case in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro; in which oxidized proteins were markedly increased. Extracellular IL-16 protein was increased in cell-free BAL fluid from chronic smokers and in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro. This was not observed in occasional smokers after short-term exposure to tobacco smoke. A marker of activation (CD69) was slightly increased whereas other markers of key cellular functions (membrane integrity, apoptosis and proliferation) in human blood CD8(+) cells in vitro were negatively affected by water-soluble tobacco smoke components. An OFR scavenger prevented these effects whereas a protein synthesis inhibitor, a beta-adrenoceptor, a glucocorticoid receptor agonist, a phosphodiesterase, a calcineurin phosphatase and a caspase-3 inhibitor did not. In conclusion, tobacco smoke depletes preformed intracellular IL-16 protein, inhibits its de novo synthesis and distorts key cellular functions in human CD8(+) cells. OFR may play a key role in this context.
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16.
  • Andersson, Anders, et al. (author)
  • Impact of tobacco smoke on interleukin-16 protein in human airways, lymphoid tissue and T lymphocytes
  • 2004
  • In: Clinical and experimental immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 138:1, s. 75-82
  • Journal article (peer-reviewed)abstract
    • CD4(+) and CD8(+) lymphocytes are mobilized in severe chronic obstructive pulmonary disease (COPD) and the CD8(+) cytokine interleukin (IL)-16 is believed to be important in regulating the recruitment and activity of CD4(+) lymphocytes. In the current study, we examined whether tobacco smoke exerts an impact not only on IL-16 in the lower airways but also in CD4(+) or CD8(+) lymphocytes or in lymphoid tissue. The concentration of IL-16 protein was measured by enzyme-linked immunosorbent assay (ELISA) in concentrated bronchoalveolar lavage fluid (BALF) collected from 33 smokers with chronic bronchitis (CB), eight asymptomatic smokers (AS) and seven healthy never-smokers (NS). The concentrations of IL-16 and soluble IL-2 receptor alpha (sIL-2Ralpha) protein were also measured in conditioned medium from human blood CD4(+) and CD8(+) lymphocytes stimulated with tobacco smoke extract (TSE) in vitro. IL-16 mRNA was assessed in vitro as well, using reverse transcription-polymerase chain reaction (RT-PCR). Finally, the intracellular immunoreactivity for IL-16 protein (IL-16IR) was assessed in six matched pairs of palatine tonsils from smokers and non-smokers. BALF IL-16 was higher in CB and AS than in NS. TSE substantially increased the concentration of IL-16 but not sIL-2Ralpha in conditioned medium from CD4(+) and CD8(+) lymphocytes. There was no corresponding effect on IL-16 mRNA. IL-16IR in tonsils was lower in smokers than in non-smokers. The current findings demonstrate that tobacco smoke exerts a wide impact on the CD8(+) cytokine IL-16, in the airway lumen, in blood CD4(+) and CD8(+) lymphocytes and in lymphoid tissue. The effect on IL-16 release may be selective for preformed IL-16 in CD4(+) lymphocytes. New clinical studies are required to evaluate whether tobacco smoke mobilizes T lymphocytes via IL-16 in the lower airways and whether this mechanism can be targeted in COPD.
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17.
  • Berg, L., et al. (author)
  • LIR-1 expression on lymphocytes, and cytomegalovirus disease in lung-transplant recipients
  • 2003
  • In: Lancet. - 0140-6736. ; 361:9363, s. 1099-101
  • Journal article (peer-reviewed)abstract
    • Human cytomegalovirus infection is a major cause of morbidity after lung transplantation. LIR-1 (leucocyte immunoglobulin-like receptor-1) is an inhibitory cell surface receptor that has high affinity for an MHC class I homologue (UL18) encoded by human cytomegalovirus. We aimed to investigate whether reactivation of human cytomegalovirus affects the expression of LIR-1. We measured LIR-1 expression on peripheral blood lymphocytes from 13 lung-transplant recipients and established human cytomegalovirus load using PCR. Eight patients developed cytomegalovirus disease. The percentage of cells expressing LIR-1 increased in the patients who developed cytomegalovirus disease several weeks before viral DNA was detectable by PCR. Measurement of LIR-1 expression might allow early identification of cytomegalovirus disease in lung-transplant patients.
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18.
  • Didon, L., et al. (author)
  • Decreased CCAAT/enhancer binding protein transcription factor activity in chronic bronchitis and COPD
  • 2005
  • In: Chest. - : Elsevier BV. - 0012-3692. ; 127:4, s. 1341-6
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: CCAAT/enhancer binding proteins (C/EBPs) are key regulators of cell differentiation and linked processes such as proliferation, apoptosis, and gene expression in several organs. C/EBPs are also central for inflammatory responses and infectious defenses, but so far little is known of their role in lung diseases. Chronic bronchitis (CB) and COPD are common smoking-associated lung diseases involving the airway epithelium. METHODS: Gelshifts were used to study C/EBP transcription factor activity in airway epithelial cells obtained by bronchial brush biopsy in four groups: healthy never-smokers (n = 10), asymptomatic smokers (n = 7), and smokers with CB and recurrent infectious exacerbations without COPD (n = 23) and with COPD (n = 13). RESULTS: C/EBP-binding activity was increased 4.6-fold in airway epithelial cells of healthy smokers compared with never-smokers. In contrast, C/EBP binding activity was not increased in the epithelium of smokers with CB or COPD. C/EBP-beta was the dominant C/EBP in the airway epithelium in all groups. CONCLUSIONS: We hypothesize that this lack of increase in C/EBP-beta activity renders the epithelium incompetent of efficient regeneration and more sensitive to infection, suggesting a previously unknown role for C/EBPs in the pathogenesis of CB and COPD.
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19.
  • Ericson, Petrea, 1966, et al. (author)
  • BAL levels of interleukin-18 do not change before or during acute rejection in lungtransplant recipients
  • 2004
  • In: Respir Med. - : Elsevier BV. - 0954-6111. ; 98:2, s. 159-63
  • Journal article (peer-reviewed)abstract
    • STUDY OBJECTIVE: Acute rejection (AR) of the allograft is a major clinical problem after lungtransplantation. Repeated episodes of AR increase the risk of developing obliterative bronchiolitis, the main cause of mortality in this patient group. It is believed that AR is caused by T-lymphocytes reacting to donor antigens and in turn activating antigen presenting cells (APC) such as alveolar macrophages. Hypothetically, the interferon-gamma inducing cytokine IL-18 released from activated macrophages can play a role in the development of AR by modulating cytotoxic T-lymphocytes. DESIGN: To determine whether IL-18 may serve as a marker of AR, we retrospectively analysed the concentration of soluble IL-18 protein and inflammatory cells in bronchoalveolar lavage fluid (BAL) from lungtransplant recipients. PATIENTS: To minimize confounding factors, eight pairs of patients were matched for age, gender, pre-op diagnosis, type of operation, absence of infection and time post transplant. METHODS: BAL levels of IL-18 (ELISA) and BAL cell differentials were analysed before, during and after an episode of AR and compared with the matched control group. CONCLUSION: We found no changes in IL-18 concentration in BAL associated with AR. IL-18 in BAL did not correlate with BAL lymphocyte percentage. We conclude that change in soluble IL-18 protein does not constitute a useful marker of acute rejection in lung allograft recipients.
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20.
  • Ericson, Petrea, 1966, et al. (author)
  • Low Levels of Exhaled Surfactant Protein A Associated With BOS After Lung Transplantation
  • 2016
  • In: Transplantation Direct. - : Ovid Technologies (Wolters Kluwer Health). - 2373-8731. ; 2:9
  • Journal article (peer-reviewed)abstract
    • Background. There is no clinically available marker for early detection or monitoring of chronic rejection in the form of bronchiolitis obliterans syndrome (BOS), the main long-term complication after lung transplantation. Sampling and analysis of particles in exhaled air is a valid, noninvasive method for monitoring surfactant protein A (SP-A) and albumin in the distal airways. Methods. We asked whether differences in composition of exhaled particles can be detected when comparing stable lung transplant recipients (LTRs) (n = 26) with LTRs who develop BOS (n = 7). A comparison between LTRs and a matching group of healthy controls (n = 33) was also conducted. Using a system developed in-house, particles were collected from exhaled air by the principal of inertial impaction before chemical analysis by immunoassays. Results. Surfactant protein A in exhaled particles and the SP-A/albumin ratio were lower (P = 0.002 and P = 0.0001 respectively) in the BOS group compared to the BOS-free group. LTRs exhaled higher amount of particles (P < 0.0001) and had lower albumin content (P < 0.0001) than healthy controls. Conclusions. We conclude that low levels of SP-A in exhaled particles are associated with increased risk of BOS in LTRs. The possibility that this noninvasive method can be used to predict BOS onset deserves further study with prospective and longitudinal approaches.
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21.
  • Glader, Pernilla, 1975, et al. (author)
  • Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space.
  • 2008
  • In: The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology. - : European Respiratory Society (ERS). - 1399-3003. ; 32:3, s. 644-650
  • Journal article (peer-reviewed)abstract
    • Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects. Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA. The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke. In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease.
  •  
22.
  • Gullestad, Lars, et al. (author)
  • Everolimus With Reduced Calcineurin Inhibitor in Thoracic Transplant Recipients With Renal Dysfunction: A Multicenter, Randomized Trial
  • 2010
  • In: Transplantation. - : Williams and Wilkins. - 0041-1337 .- 1534-6080. ; 89:7, s. 864-872
  • Journal article (peer-reviewed)abstract
    • Background. The proliferation signal inhibitor everolimus offers the potential to reduce calcineurin inhibitor (CNI) exposure and alleviate CNI-related nephrotoxicity. Randomized trials in maintenance thoracic transplant patients are lacking. Methods. In a 12-month, open-labeled, multicenter study, maintenance thoracic transplant patients (glomerular filtration rate greater than= 20 mL/min/1.73m(2) and less than90 mL/min/1.73 m(2)) greater than1 year posttransplant were randomized to continue their current CNI-based immunosuppression or start everolimus with predefined CNI exposure reduction. Results. Two hundred eighty-two patients were randomized (140 everolimus, 142 controls; 190 heart, 92 lung transplants). From baseline to month 12, mean cyclosporine and tacrolimus trough levels in the everolimus cohort decreased by 57% and 56%, respectively. The primary endpoint, mean change in measured glomerular filtration rate from baseline to month 12, was 4.6 mL/min with everolimus and -0.5 mL/min in controls (Pless than0.0001). Everolimus-treated heart and lung transplant patients in the lowest tertile for time posttransplant exhibited mean increases of 7.8 mL/min and 4.9 mL/min, respectively. Biopsy-proven treated acute rejection occurred in six everolimus and four control heart transplant patients (P=0.54). In total, 138 everolimus patients (98.6%) and 127 control patients (89.4%) experienced one or more adverse event (P=0.002). Serious adverse events occurred in 66 everolimus patients (46.8%) and 44 controls (31.0%) (P=0.02). Conclusion. Introduction of everolimus with CNI reduction offers a significant improvement in renal function in maintenance heart and lung transplant recipients. The greatest benefit is observed in patients with a shorter time since transplantation.
  •  
23.
  • Gullestad, Lars, et al. (author)
  • Two-Year Outcomes in Thoracic Transplant Recipients After Conversion to Everolimus With Reduced Calcineurin Inhibitor Within a Multicenter, Open-Label, Randomized Trial.
  • 2010
  • In: Transplantation. - : Williams and Wilkins. - 1534-6080 .- 0041-1337. ; 90:12, s. 1581-1589
  • Journal article (peer-reviewed)abstract
    • BACKGROUND.: Use of the mammalian target of rapamycin inhibitor everolimus with an accompanying reduction in calcineurin inhibitor (CNI) exposure has shown promise in preserving renal function in maintenance thoracic transplant patients, but robust, long-term data are required. METHODS.: In a prospective, open-label, multicenter study, thoracic transplant recipients more than or equal to 1 year posttransplant with mild-to-moderate renal insufficiency were randomized to continue their current CNI-based immunosuppression or convert to everolimus with predefined CNI exposure reduction. After a 12-month core trial, patients were followed up to month 24 after randomization. RESULTS.: Of 245 patients who completed the month 12 visit, 235 patients (108 everolimus and 127 controls) entered the 12-month extension phase. At month 24, mean measured glomerular filtration rate had increased by 3.2±12.3 mL/min from the point of randomization in everolimus-treated patients and decreased by 2.4±9.0 mL/min in controls (P<0.001), a difference that was significant within both the heart and lung transplant subpopulations. During months 12 to 24, 5.6% of everolimus patients and 3.1% of controls experienced biopsy-proven acute rejection (P=0.76). There were no significant differences in the rate of adverse events or serious adverse events (including pneumonia) between groups during months 12 to 24. CONCLUSIONS.: Converting maintenance thoracic transplant recipients to everolimus with low-exposure CNI results in a renal benefit that is sustained to 2 years postconversion, with significantly improved measured glomerular filtration rate in both heart and lung transplant patients. Despite reductions of more than 50% in CNI exposure, there was no marked loss of efficacy. The safety profile of the everolimus-based regimen was acceptable.
  •  
24.
  • Hammarström, Helena, et al. (author)
  • Fungal Tracheobronchitis in Lung Transplant Recipients : Incidence and Utility of Diagnostic Markers
  • 2023
  • In: Journal of Fungi. - : MDPI AG. - 2309-608X. ; 9:1
  • Journal article (peer-reviewed)abstract
    • Fungal tracheobronchitis caused by Aspergillus and Candida spp. is a recognized complication after lung transplantation, but knowledge of the incidence of Candida tracheobronchitis is lacking. The diagnosis relies on fungal cultures in bronchoalveolar lavage fluid (BALF), but cultures have low specificity. We aimed to evaluate the one-year incidence of fungal tracheobronchitis after lung transplantation and to assess the utility of diagnostic markers in serum and BALF to discriminate fungal tracheobronchitis from colonization. Ninety-seven consecutively included adult lung-transplant recipients were prospectively followed. BALF and serum samples were collected at 1, 3 and 12 months after transplantation and analyzed for betaglucan (serum and BALF), neutrophils (BALF) and galactomannan (BALF). Fungal tracheobronchitis was defined according to consensus criteria, modified to include Candida as a mycologic criterion. The cumulative one-year incidence of Candida and Aspergillus tracheobronchitis was 23% and 16%, respectively. Neutrophils of >75% of total leukocytes in BALF had 92% specificity for Candida tracheobronchitis. The area under the ROC curves for betaglucan and galactomannan in BALF to discriminate Aspergillus tracheobronchitis from colonization or no fungal infection were high (0.86 (p < 0.0001) and 0.93 (p < 0.0001), respectively). To conclude, the one-year incidence of fungal tracheobronchitis after lung transplantation was high and dominated by Candida spp. Diagnostic markers in BALF could be useful to discriminate fungal colonization from tracheobronchitis.
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25.
  • Kjellström, Christer, 1955, et al. (author)
  • The origin of alveolar macrophages in the transplanted lung: a longitudinal microsatellite-based study of donor and recipient DNA
  • 2000
  • In: Transplantation. - 0041-1337. ; 69:9, s. 1984-6
  • Journal article (peer-reviewed)abstract
    • Transplanted lungs are initially populated by donor pulmonary alveolar macrophages (PAMs). These will form major antigen presenters for the recipient's suppressed immune system. They may be expected to be replaced by recipient major histocompatibility complex-compatible cells, with time. We have isolated CD14+ PAMs from bronchoalveolar lavage specimens for 6 months after transplantation and identified their origin by using microsatellite analysis. This DNA-based technology permits the reliable identification of the origin of cells from different individuals. We show that replacement of donor PAMs occurs with individual dynamics in each case. Recipient PAMs usually appeared within 2 weeks, whereas donor cells could be retained for as long as 6 months. In this limited series, there was no obvious correlation between the dynamics of this process and the occurrence of rejection episodes or infections.
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26.
  • Laan, Martti, 1971, et al. (author)
  • IL-16 in the airways of lung allograft recipients with acute rejection or obliterative bronchiolitis
  • 2003
  • In: Clin Exp Immunol. - 0009-9104. ; 133:2, s. 290-6
  • Journal article (peer-reviewed)abstract
    • Acute rejection (AR) is the principal risk factor for obliterative bronchiolitis (OB), the major complication of lung transplantation. It is known that activated CD4+ T lymphocytes are involved in the development of AR and that interleukin (IL)-16 can inhibit the activity of CD4+ T lymphocytes. In this study, we evaluated whether the concentration of IL-16 in the airways is altered in AR or OB and, if so, how this IL-16 concentration relates to the number or activity of airway lymphocytes. The concentration of IL-16 protein was measured in bronchoalveolar lavage (BAL) fluid at three time-points in lung allograft recipients with either AR or OB and in matched controls using ELISA. The concentration of soluble IL-2 receptor (R) protein was measured in BAL fluid using ELISA as well, as an indicator of lymphocyte activity. The percentage of airway lymphocytes was evaluated by performing BAL differential cell counts. Lung allograft recipients with AR displayed lower IL-16 concentrations compared with matched control patients and this IL-16 concentration correlated negatively with the sIL-2R concentration, but it did not correlate with the percentage of lymphocytes in BAL fluid. In contrast, in BAL fluid from lung allograft recipients with OB, the IL-16 concentration was not altered compared with matched control patients and it did not correlate with the percentage of lymphocytes or with the sIL-2R concentration. These data are compatible with an increase in IL-16 playing a protective role against AR but not against OB and, hypothetically, this type of protective effect could be exerted via a down-regulation of the activity of T lymphocytes.
  •  
27.
  • Laan, Martti, 1971, et al. (author)
  • Increased levels of interleukin-16 in the airways of tobacco smokers: relationship with peripheral blood T lymphocytes
  • 1999
  • In: Thorax. - 0040-6376. ; 54:10, s. 911-6
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: The mechanisms behind the development of systemic immunomodulation among tobacco smokers are not fully understood, but several studies have indicated a role for CD8+ and/or CD4+ T cells. Interleukin (IL)-16, a cytokine released from inflammatory cells as well as bronchial epithelial cells, can recruit and activate CD4+ T cells. A study was undertaken to establish whether the IL-16 level is increased in the airways of tobacco smokers and to determine whether airway levels of IL-16 are related to the number and function of systemic T lymphocytes. METHODS: Bronchoalveolar lavage (BAL) fluid was collected from eight never smokers and 18 tobacco smokers without clinical airway symptoms, and from 16 tobacco smokers with clinical airway symptoms. Interleukin-16 protein levels in BAL fluid were determined using enzyme-linked immunosorbent assay (ELISA). Peripheral blood was collected for determination of CD4+ T cell content using flow cytometry. The responsiveness of systemic lymphocytes in smokers was assessed by measuring the proliferative response of peripheral blood lymphocytes to the superantigen staphylococcus enterotoxin A (SEA). RESULTS: The IL-16 protein level in the BAL fluid was significantly higher in tobacco smokers than in non-smokers. However, among tobacco smokers the IL-16 level was similar in asymptomatic smokers and in those with airway symptoms. The level of IL-16 in the BAL fluid of smokers correlated negatively with the percentage of CD4+ T cells and positively with superantigen stimulated lymphocyte proliferation in peripheral blood. CONCLUSIONS: In tobacco smokers the airway IL-16 level is increased and it is possible that this increase in IL-16 influences systemic immunomodulation by altering the number and responsiveness of systemic T lymphocytes.
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28.
  • Magnusson, Jesper, et al. (author)
  • Incidence of Hepatitis E Antibodies in Swedish Lung Transplant Recipients
  • 2015
  • In: Transplantation Proceedings. - : Elsevier BV. - 0041-1345. ; 47:6, s. 1972-1976
  • Journal article (peer-reviewed)abstract
    • Background. Hepatitis E virus (REV) is an important cause of acute and chronic hepatitis in solid organ transplant recipients, especially liver transplant recipients. However, less is known of the incidence and prevalence of HEV in lung transplant recipients. Methods. In a prospective study, 62 patients were observed during the first year after lung transplantation. Sera were analyzed for anti-REV immunoglobulin G (IgG) and IgM at 12 months after transplantation. Samples positive for anti-REV were also analyzed for REV RNA by polymerase chain reaction. Pretransplantation samples were analyzed for patients with detectable anti-REV 1 year after transplantation. Results. Eight patients (13%) had anti-REV IgG at the 12-month follow-up sample. HEV RNA could not be detected in any of these samples. One of these patients seroconverted during the follow-up without developing acute or chronic hepatitis. Conclusions. Our results show that the prevalence of REV antibodies among Swedish lung transplant recipients is similar when compared to the general population. It also suggests that the risk for REV antibody seroconversion during first year is limited.
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29.
  • Magnusson, Jesper, et al. (author)
  • Involvement of IL-26 in bronchiolitis obliterans syndrome but not in acute rejection after lung transplantation
  • 2022
  • In: Respiratory Research. - : Springer Science and Business Media LLC. - 1465-993X. ; 23:1
  • Journal article (peer-reviewed)abstract
    • Background The main long-term complication after lung transplantation is bronchiolitis obliterans syndrome (BOS), a deadly condition in which neutrophils may play a critical pathophysiological role. Recent studies show that the cytokine interleukin IL-26 can facilitate neutrophil recruitment in response to pro-inflammatory stimuli in the airways. In this pilot study, we characterized the local involvement of IL-26 during BOS and acute rejection (AR) in human patients. Method From a biobank containing bronchoalveolar lavage (BAL) samples from 148 lung transplant recipients (LTR), clinically-matched patient pairs were identified to minimize the influence of clinical confounders. We identified ten pairs (BOS/non-BOS) with BAL samples harvested on three occasions for our longitudinal investigation and 12 pairs of patients with and without AR. The pairs were matched for age, gender, preoperative diagnosis, type of and time after surgery. Extracellular IL-26 protein was quantified in cell-free BAL samples using an enzyme-linked immunosorbent assay. Intracellular IL-26 protein in BAL cells was determined using immunocytochemistry (ICC) and flow cytometry. Results The median extracellular concentration of IL-26 protein was markedly increased in BAL samples from patients with BOS (p < 0.0001) but not in samples from patients with AR. Intracellular IL-26 protein was confirmed in alveolar macrophages and lymphocytes (through ICC and flow cytometry) among BAL cells obtained from BOS patients. Conclusions Local IL-26 seems to be involved in BOS but not AR, and macrophages as well as lymphocytes constitute cellular sources in this clinical setting. The enhancement of extracellular IL-26 protein in LTRs with BOS warrants further investigation of its potential as a target for diagnosing, monitoring, and treating BOS.
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30.
  • Magnusson, Jesper, et al. (author)
  • Long-term Extracorporeal Membrane Oxygenation Bridge to Lung Transplantation After COVID-19
  • 2022
  • In: Annals of Thoracic Surgery. - : Elsevier BV. - 0003-4975 .- 1552-6259. ; 113:1
  • Journal article (peer-reviewed)abstract
    • This report describes a patient with severe acute respiratory syndrome coronavirus 2 infection and irreversible lung destruction who underwent successful lung transplantation after 138 days of bridging with extracorporeal membrane oxygenation support. The case exemplifies that lung transplantation may be a possibility after very long-term coronavirus disease 2019 care, even if the patient is initially an unsuitable candidate. (C) 2022 by The Society of Thoracic Surgeons. Published by Elsevier Inc.
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31.
  • Magnusson, Jesper, et al. (author)
  • The Impact of Viral Respiratory Tract Infections on Long-Term Morbidity and Mortality following Lung Transplantation: A Retrospective Cohort Study Using a Multiplex PCR Panel.
  • 2013
  • In: Transplantation. - 1534-6080. ; 95:2, s. 383-388
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: The major factor affecting morbidity and mortality after lung transplantation (LTX) is bronchiolitis obliterans syndrome. Earlier studies have suggested a connection between the presence of viral agents and morbidity in this patient group, but data are somewhat conflicting. The objective of this study was to investigate the development of bronchiolitis obliterans syndrome and graft loss after LTX in relation to the presence of respiratory viruses during the first year after LTX. METHOD: The study is a retrospective cohort study of 39 LTX recipients 11-13 years after surgery. Patients were operated between January 1, 1998 and December 31, 2000 at Sahlgrenska University Hospital. The presence of virus in bronchoalveolar lavage (BAL) fluids from patients during the first year after surgery was analyzed retrospectively using a multiplex polymerase chain reaction test capable of detecting 15 respiratory agents. The time to BOS or graft loss was analyzed in relation to the positive findings in BAL during the first year after LTX. RESULTS: Patients with one or more viruses detected in BAL during the first year after transplantation demonstrated a significantly faster development of BOS (P=0.005) compared with patients with no virus detected. No significant difference in graft survival was found. CONCLUSION: Our results suggest that the long-term prognosis after LTX may be negatively affected by viral respiratory tract infections during the first year after LTX.
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32.
  • Magnusson, Jesper, et al. (author)
  • Viral Respiratory Tract Infection During the First Postoperative Year Is a Risk Factor for Chronic Rejection After Lung Transplantation
  • 2018
  • In: Transplantation Direct. - : Ovid Technologies (Wolters Kluwer Health). - 2373-8731. ; 4:8
  • Journal article (peer-reviewed)abstract
    • Background. Chronic lung allograft dysfunction (CLAD) is the major limiting factor for long-term survival in lung transplant recipients. Viral respiratory tract infection (VRTI) has been previously associated with CLAD development. The main purpose of this study was to evaluate the long-term effects of VRTI during the first year after lung transplantation in relation to CLAD development. Method. Ninety-eight patients undergoing lung transplantation were prospectively enrolled between 2009 and 2012. They were monitored for infections with predefined intervals and on extra visits during the first year, the total follow-up period ranged between 5 and 8 years. Nasopharyngeal swab and bronchoalveolar lavage samples were analyzed using a multiplex polymerase chain reaction panel for respiratory pathogens. Data regarding clinical characteristics and infectious events were recorded. Results. Viral respiratory tract infection during the first year was identified as a risk factor for long-term CLAD development (P = 0.041, hazard ratio 1.94 [1.03-3.66]) in a time-dependent multivariate Cox regression analysis. We also found that coronavirus in particular was associated with increased risk for CLAD development. Other identified risk factors were acute rejection and cyclosporine treatment. Conclusions. This study suggests that VRTI during the first year after lung transplantation is associated with long-term CLAD development and that coronavirus infections in particular might be a risk factor.
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33.
  • Nord, M., et al. (author)
  • Decreased serum and bronchoalveolar lavage levels of Clara cell secretory protein (CC16) is associated with bronchiolitis obliterans syndrome and airway neutrophilia in lung transplant recipients
  • 2002
  • In: Transplantation. - : Ovid Technologies (Wolters Kluwer Health). - 0041-1337. ; 73:8, s. 1264-9
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: The major hinderance for long-term survival after lung transplantation is chronic rejection in the form of bronchiolitis obliterans syndrome (BOS). BOS is a fibrosing process in the small airways causing irreversible airway obstruction. BOS is associated with increased oxidative burden and activation of inflammatory and growth-stimulating mediators. The Clara cell secretory protein (CCSP or CC16) is a secreted differentiation marker for the bronchiolar epithelium with both antioxidative and antiinflammatory/immmunomodulatory properties. We asked whether this molecule could have a role in the development of BOS. METHODS: Serum and bronchoalveolar lavage (BAL) fluid samples were collected from 22 consecutive lung transplant recipients, the majority (19) was followed for 2 years. Six patients developed BOS. CCSP in serum was measured in 162 samples from 19 patients with an ELISA method, and CCSP in 191 BAL samples from 22 patients with quantitative Western blot. RESULTS: CCSP in both serum and BAL was significantly lower in BOS compared with acute rejection or no rejection. After the first postoperative month, serum and BAL CCSP levels were consistently lower in the patients who developed BOS than in those who did not. The percentage of neutrophils in BAL correlated negatively with CCSP in BAL. CONCLUSIONS: Levels of CCSP in serum and BAL is lowered in BOS. Serum CCSP could have a potential as an early marker for BOS. The correlation between decreased CCSP and increased neutrophils in BAL suggests a loss of local airway defense capacity in BOS.
  •  
34.
  •  
35.
  • Qvarfordt, Ingemar, 1954, et al. (author)
  • Cutaneous delayed-type hypersensitivity reactions in smokers with chronic bronchitis and recurrent exacerbations: comparison with asymptomatic smokers and never-smokers
  • 1999
  • In: Respir Med. - 0954-6111. ; 93:7, s. 491-7
  • Journal article (peer-reviewed)abstract
    • The aim of the present study was to investigate whether smoking patients with chronic bronchitis (CB) and recurrent exacerbations show signs of depressed cell-mediated immunity (CMI), as reflected in the cutaneous delayed-type hypersensitivity (DTH) reaction, in comparison with asymptomatic smokers and healthy never-smokers. The study was a comparative clinical study performed at a university hospital center of respiratory medicine. Sixteen smokers with stable CB and recurrent exacerbations, five of whom had mild airflow obstruction, 18 asymptomatic smokers and 18 healthy never-smokers, all aged between 35 and 64 years, participated. No subjects treated with corticosteroids or N-acetylcysteine were included. Cutaneous DTH-reactions to seven recall antigens were assessed with Multitest, a standardized in vivo test of clinical CMI. Reactions were assessed 48 h after application by measurement of skin induration. A score (sum in mm of positive reactions) was created to assess overall reactivity. Neither the score nor the number of positive reactions differed significantly between the three study groups. Men had a significantly higher reactivity than women (P < 0.05) irrespective of group affiliation. No influence of smoking status on DTH reactivity could be seen. In the CB group no correlation was found between DTH reactivity and number of exacerbations the past 2 years. Patients with chronic bronchitis and recurrent exacerbations did not differ from asymptomatic smokers or healthy never-smokers with respect to cutaneous DTH reactions. Depression of CMI, as measured in this study, does not seem to be a primary factor behind recurrent exacerbations in smokers with CB.
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36.
  • Qvarfordt, Ingemar, 1954, et al. (author)
  • IgG subclasses in smokers with chronic bronchitis and recurrent exacerbations
  • 2001
  • In: Thorax. - 0040-6376. ; 56:6, s. 445-9
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Tobacco smokers have lower serum levels of IgG than non-smokers. IgG subclass deficiency is common in patients with recurrent respiratory infections. Recurrent bronchial infections are common in smokers with chronic bronchitis (CB). We have investigated whether susceptibility to recurrent exacerbations in smokers with CB is associated with altered IgG subclass levels or IgG subclass deficiency. METHODS: Serum levels of IgG, IgA, IgM, and IgG subclasses 1-4 were determined by radial immunodiffusion in 100 subjects: 33 smokers with stable CB and recurrent exacerbations, 24 asymptomatic smokers, and 43 healthy never smokers. Systemic tobacco exposure was verified and excluded using a serum cotinine ELISA. Immunoglobulin data were log transformed to enable use of parametric statistical methods. RESULTS: Compared with never smokers, both patients with CB and asymptomatic smokers had significantly lower levels of IgG (median 9.7 g/l (range 5.6-15.2) and 9.9 (6.1-12.1) g/l v 12.0 (6.9-18.5) g/l) and IgG2 (2.8 (0.9-5.9) g/l and 2.5 (1.0-6.3) g/l v 4.0 (1.7-10.2) g/l). The estimated ratio of median values between the patients with CB and never smokers was 0.78 (95% confidence interval (CI) 0.69 to 0.89) for IgG and 0.65 (95% CI 0.50 to 0.83) for IgG2. The corresponding ratios between asymptomatic smokers and never smokers were 0.79 (95% CI 0.69 to 0.91) and 0.60 (95% CI 0.50 to 0.83), respectively. There were no significant differences between the smoking groups. CONCLUSIONS: Susceptibility to recurrent exacerbations in smokers with CB is not associated with lower levels of IgG subclasses than can be accounted for by smoking per se.
  •  
37.
  • Qvarfordt, Ingemar, 1954, et al. (author)
  • Immunological findings in blood and bronchoalveolar lavage fluid in chronic bronchitis patients with recurrent infectious exacerbations
  • 1998
  • In: Eur Respir J. - 0903-1936. ; 11:1, s. 46-54
  • Journal article (peer-reviewed)abstract
    • Bronchial infections are common in smokers and seem to be related to the presence of chronic bronchitis (CB). Why only some smokers develop repeated bronchial infections is not known. The aim of this study was to screen for immunological changes associated with disease in patients with CB and recurrent infectious exacerbations compared to asymptomatic smokers. Sixteen smokers with stable CB and recurrent infectious exacerbations, and 18 asymptomatic smokers, all without any immunomodulating treatment, underwent bronchoscopy and bronchoalveolar lavage (BAL). Smoking history and current smoking status were comparable. Serum levels of immunoglobulin (Ig)A, IgM, IgG and IgG subclasses were measured. Blood and BAL lymphocyte phenotypes and proliferative responses of peripheral blood mononuclear cells (PBMCs) to various stimulators were analysed. Unstimulated and tetanus toxoid-stimulated production of cytokines in PBMC cultures was measured. Natural killer (NK-) cell activity was analysed. A significantly (p<0.05) lower level of IgG3 was found in the CB group, and a significantly (p<0.01) higher proliferative response of PBMCs was found in the CB group after stimulation with diphtheria toxoid. Detectable levels of interleukin (IL)-6, tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma, but not of IL-2, IL-4 or transforming growth factor-beta2, were found in supernatants from cultured cells in both study groups. Stimulated TNF-alpha production was significantly (p<0.05) higher in the CB group. NK-cell activity did not differ significantly between the study groups. There were no major differences between the groups in lymphocyte subpopulations in blood or BAL. In conclusion, no major alterations in the analysed indices of cell-mediated and humoral immunity were found in patients with chronic bronchitis prone to recurrent infectious exacerbations when compared with asymptomatic smoking controls.
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38.
  • Qvarfordt, Ingemar, 1954, et al. (author)
  • Lower airway bacterial colonization in asymptomatic smokers and smokers with chronic bronchitis and recurrent exacerbations
  • 2000
  • In: Respir Med. - 0954-6111. ; 94:9, s. 881-7
  • Journal article (peer-reviewed)abstract
    • Bacterial colonization of the lower airways in patients with chronic bronchitis (CB) has been described mainly in patients with co-existing chronic obstructive pulmonary disease (COPD). Although smoking has been identified as a risk factor for bacterial colonization it is not known whether asymptomatic smokers (AS) can be colonized. The aim of this study was to study lower airway bacterial colonization in smokers with stable CB and recurrent exacerbations and compare with AS and healthy never-smokers (NS). Thirty-nine smokers with CB and recurrent exacerbations (median FEV1 85% of predicted normal), 10 AS and 10 NS, underwent bronchoscopy and a two-step bronchoalveolar lavage (BAL) procedure where the first portion (20 ml, 'pre-BAL') was recovered separately from the rest (140 ml, 'BAL'). The degree of oropharyngeal contamination of pre-BAL and BAL samples was evaluated by cytology. Semiquantitative bacterial cultures were performed on all samples. Higher bacterial numbers than 10(3) colony-forming units (cfu) x ml(-1) in BAL were found only in the two smoking groups. Using 10(3) cfu x ml(-1) as cut-off, 6/10 (60%) in the AS-, and 7/35 (20%) in the CB-group were colonized in the lower airways. In all, 29% of all smokers had bacterial colonization. Only bacteria belonging to the normal oropharyngeal flora were found. The proportion of samples with oropharyngeal contamination was significantly lower in BAL than in pre-BAL (5% vs. 21%, P=0.039). The proportion of sterile samples was significantly higher in BAL than in pre-BAL (49% vs. 26%, P=0.002). Lower airway bacterial colonization was found both in asymptomatic smokers and in patients with CB. Colonization with potential respiratory pathogens is uncommon in patients with CB and recurrent exacerbations without severe airflow obstruction. The two-step BAL procedure seems to decrease oropharyngeal contamination.
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39.
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40.
  • Riise, Gerdt C., 1956, et al. (author)
  • A bronchoscopic brush biopsy study of large airway mucosal pathology in smokers with chronic bronchitis and in healthy nonsmokers
  • 1992
  • In: Eur Respir J. - 0903-1936. ; 5:4, s. 382-6
  • Journal article (peer-reviewed)abstract
    • We investigated the use of bronchial brush biopsies of the bronchial epithelium as a diagnostic tool in common airway diseases. Flexible fibreoptic bronchoscopy was performed on 22 smokers with nonobstructive chronic bronchitis and on 14 healthy nonsmoking individuals. Ten of the smokers had recurrent infectious exacerbations. Cell samples were taken from carinal and subsegmental levels of the bronchial tree with a standard cytological brush, and a differential count was made of the different cell types. Smokers with chronic bronchitis had significantly more goblet cells (mean 20.0, SD 8.6), and less ciliated epithelial cells (mean 74.1, SD 9.4), than the healthy nonsmokers (mean 9.2, SD 3.9 and mean 84.7, SD 6.6, respectively). No such changes were found between the chronic bronchitis groups with or without infectious exacerbations. Thus, bronchial brush biopsies can be used as a complement to standard bronchial biopsies in the investigation of airway diseases other than pulmonary malignancies.
  •  
41.
  • Riise, Gerdt C., 1956, et al. (author)
  • Bacterial adhesion to oropharyngeal and bronchial epithelial cells in smokers with chronic bronchitis and in healthy nonsmokers
  • 1994
  • In: Eur Respir J. - 0903-1936. ; 7:10, s. 1759-64
  • Journal article (peer-reviewed)abstract
    • Bacterial adhesion is probably a prerequisite for colonization of mucous membranes, but adhesion to the bronchial mucosa has not been studied in detail. We investigated adhesion of respiratory pathogens to bronchial epithelial cells, and asked whether chronic bronchitis had an influence on bacterial adhesion. Oropharyngeal and bronchial cells were collected during bronchoscopy from 14 healthy nonsmokers, 22 smokers with nonobstructive chronic bronchitis, and 19 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD). Patients with a forced expiratory volume in one second (FEV1) less than 50% predicted were excluded. Adhesion of highly adherent test strains of H. influenzae and S. pneumoniae to these cells were studied. The test strains of H. influenzae and S. pneumoniae were found to adhere well to both oropharyngeal and bronchial cells. H. influenzae showed a higher degree of adhesion both to ciliated and goblet cells from the patients with nonobstructive bronchitis than to cells from the healthy nonsmokers. No corresponding difference was found for S. pneumoniae. The patients with COPD did not differ from the controls in their adhesion values. Our results indicate that bacterial adhesion is of importance for the colonization and retention of H. influenzae in the human airways. For S. pneumoniae the role of adhesion is more uncertain.
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42.
  • Riise, Gerdt C., 1956, et al. (author)
  • Bronchial brush biopsies for studies of epithelial inflammation in stable asthma and nonobstructive chronic bronchitis
  • 1996
  • In: Eur Respir J. - 0903-1936. ; 9:8, s. 1665-71
  • Journal article (peer-reviewed)abstract
    • Recently, bronchial brush biopsy (BBB) has been introduced as a complimentary method to bronchial forceps biopsy for the study of bronchial epithelial cells. We wanted to determine whether epithelial inflammatory cells in bronchial brush biopsies can reflect mucosal inflammation assessed indirectly by levels of cellular activation markers in bronchial lavage fluid. We studied 15 healthy controls, 11 asthmatics with regular steroid inhalation therapy, 13 asthmatics without steroids, and 10 smokers with nonobstructive chronic bronchitis. Differential counts of epithelial and inflammatory cells were made from the BBB material. Bronchial lavage levels of eosinophil cationic protein (ECP), myeloperoxidase (MPO), tryptase, hyaluronan and interleukin-8 (IL-8) were measured as indirect markers for inflammatory cell activation. We found an increased percentage of eosinophil granulocytes in the BBB from the steroid-untreated asthmatic patients (1.16%) in comparison to the other groups (0.11%, 0.09% and 0.02%, respectively; p<0.01). In the steroid-untreated asthmatic patients, the percentage of eosinophils correlated with ECP in bronchial lavage fluid (r=0.73; p<0.01), indicating that the BBB method can reflect the degree of eosinophilic activation. A negative correlation was found for the percentage of eosinophils in BBB with levels of provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (PC20) for the asthmatic patients in the study (r= -0.67; p<0.003). The bronchial brush biopsy method appears to give information on the changes present in superficial bronchial epithelium in inflammatory airways disease. These changes appear to relate to the degree of inflammatory activity and disease severity in asthma.
  •  
43.
  • Riise, Gerdt C., 1956, et al. (author)
  • Bronchial inflammation in chronic bronchitis assessed by measurement of cell products in bronchial lavage fluid
  • 1995
  • In: Thorax. - 0040-6376. ; 50:4, s. 360-5
  • Journal article (peer-reviewed)abstract
    • BACKGROUND--Bronchial inflammation in chronic bronchitis has not been characterised as well as in asthma. The present study was undertaken to assess whether a characteristic pattern of bronchial inflammatory markers could be found in patients with chronic bronchitis. METHODS--Bronchoscopy with bronchial lavage was performed in 42 patients with chronic bronchitis and in 13 healthy controls. Twenty three of the patients had non-obstructive chronic bronchitis and 19 had chronic bronchitis and chronic obstructive pulmonary disease (COPD). Eighteen of the patients with bronchitis had recurrent infective exacerbations and 24 did not. Intrabronchial bacterial cultures were taken with a protected specimen brush. RESULTS--Increased activity of neutrophils, fibroblasts, and eosinophils was found in the patients with chronic bronchitis as assessed by the levels of myeloperoxidase (MPO) and interleukin-8 (IL-8), hyaluronan, and eosinophil cationic protein (ECP), respectively. The levels of tryptase did not differ from the controls. High correlations were found between the levels of MPO and IL-8, as well as ECP and IL-8. No differences were found between the patients with COPD and those with non-obstructive chronic bronchitis. CONCLUSIONS--Recruitment and activation of both neutrophils and eosinophils seem to be a characteristic of chronic bronchitis. This activation is associated with IL-8. The patients with intrabronchial cultures of Streptococcus pneumoniae had the highest individual levels of MPO, ECP, and IL-8 of all subjects in the study, indicating that colonisation with S pneumoniae could promote bronchial inflammation.
  •  
44.
  •  
45.
  • Riise, Gerdt C., 1956, et al. (author)
  • Circulating cell adhesion molecules in bronchial lavage and serum in COPD patients with chronic bronchitis
  • 1994
  • In: Eur Respir J. - 0903-1936. ; 7:9, s. 1673-1677
  • Journal article (peer-reviewed)abstract
    • The initial phase of inflammation in bronchial asthma appears to be triggered by the expression of leucocyte-endothelial adhesion molecules on endothelial cell surfaces. Cell adhesion molecules (CAMs) cause adhesion of leucocytes to the endothelium prior to their subsequent extravasation into inflamed tissue. We wanted to determine whether circulating intercellular adhesion molecule-1 (cICAM-1) and circulating E-selectin (cE-selectin) could be detected in bronchial lavage fluid and serum in patients with stable chronic obstructive pulmonary disease (COPD) and chronic bronchitis. Bronchoscopy and small volume bronchial lavage was performed in 19 patients with COPD and chronic bronchitis and in 13 control subjects. We found increased mean levels of cICAM-1 both in serum (481 micrograms.l-1) and in bronchial lavage (24 micrograms.l-1) in the COPD patients as compared to the controls (321 micrograms.l-1 in serum, 15 micrograms.l-1 in lavage). We also found higher mean levels of cE-selectin in serum from the COPD patients (86 micrograms.l-1) compared to controls (50 micrograms.l-1). The serum levels of cE-selectin correlated significantly with lung function measured as forced expiratory volume in one second (FEV1) in percentage of predicted. Patients with significant intrabronchial bacterial colonization had increased levels of serum cE-selectin. Our results indicate that cCAMs may reflect an upregulation of CAMs on endothelial and epithelial airway cells in COPD.
  •  
46.
  • Riise, Gerdt C., 1956, et al. (author)
  • Circulating leukocyte adhesion molecules in stable asthma and nonobstructive chronic bronchitis
  • 1995
  • In: Allergy. - 0105-4538. ; 50:8, s. 693-8
  • Journal article (peer-reviewed)abstract
    • Leukocyte adhesion molecules have been associated with airway inflammatory diseases such as asthma and obstructive chronic bronchitis. Lately, it has become possible to measure circulating forms of cell adhesion molecules (cCAMs) in body fluids. Elevated serum levels have been found in acute asthma and in obstructive chronic bronchitis. We investigated whether the patterns of cICAM-1, cVCAM-1, and cE-selectin could serve as markers for airway inflammation in stable asthma and stable nonobstructive chronic bronchitis. Small-volume bronchial lavage (BL) and serum from 15 controls, 13 asthmatics without steroid inhalation therapy, 11 asthmatics with regular steroid inhalation therapy, and 10 smokers with chronic bronchitis were analyzed. We found cICAM-1, cVCAM-1, and cE-selectin to be present in serum from patients with stable asthma and stable nonobstructive chronic bronchitis. Only cICAM-1 was found in BL fluid. No differences were seen between the subject groups for either cCAM, but levels of ECP were increased in the non-steroid-treated asthmatic group. Subject atopy or smoking did not increase the cCAM levels. In conclusion, the degree of airway inflammation in stable nonobstructive chronic bronchitis and stable asthma does not appear to be well associated with circulating ICAM-1, cVCAM-1, and cE-selectin.
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47.
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48.
  • Riise, Gerdt C., 1956, et al. (author)
  • Increased net gelatinase but not serine protease activity in bronchiolitis obliterans syndrome.
  • 2010
  • In: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. - : Elsevier BV. - 1557-3117. ; 29:7, s. 800-7
  • Journal article (peer-reviewed)abstract
    • Bronchiolitis obliterans syndrome (BOS) is the main long-term complication after lung transplantation. Previous studies indicate that neutrophil mobilization causes high protease concentrations in the lung allograft during BOS. This study assessed net protease activity and the functional aspect of proteases in BOS.
  •  
49.
  • Riise, Gerdt C., 1956, et al. (author)
  • Infektioner och astma
  • 2005
  • In: Larsson K; Astma hos vuxna. Förekomst, sjukdomsbild, diagnostik och behandling.. - Södertälje : Astra Zeneca, Hjärt-Lungfonden. - 9186056484 ; , s. 113-30
  • Book chapter (other academic/artistic)
  •  
50.
  • Riise, Gerdt C., 1956, et al. (author)
  • Infektioner och astma
  • 1996
  • In: Astma – klinik och behandling. - Lund : Draco Läkemedel AB och Hjärt-Lungfonden. ; , s. 27-42
  • Book chapter (other academic/artistic)
  •  
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