| 1. |
- Barck, Charlotte, et al.
(författare)
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Does nitrogen dioxide affect inflammatory markers after nasal allergen challenge?
- 2005
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Ingår i: American Journal of Rhinology. - : SAGE Publications. - 1050-6586 .- 1539-6290. ; 19:6, s. 560-566
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Exposure to high ambient levels of nitrogen dioxide (NO2) enhances the bronchial inflammatory reaction to allergen in humans. We tested whether this NO2 effect occurs also in the upper airways. METHODS: Sixteen allergic subjects with rhinitis and mild asthma were exposed at rest to either purified air or 500 microg/m3 NO2 for 30 minutes, followed 4 hours later by a nasal allergen challenge. Nasal lavage was performed before air/NO2 exposure, before allergen challenge, and 1, 4 and 18 hours after allergen challenge. Symptoms were recorded. RESULTS: The percentage of eosinophils and neutrophils, eosinophil cationic protein, and myeloperoxidase were similar after exposure to air + allergen and to NO2 + allergen. We noticed a tendency to increased sneezing the day after exposure to NO2 + allergen. CONCLUSION: The priming effect of an ambient brief NO2 exposure on subsequent allergic response was not noticeable in activation of inflammatory cells and mediators in the upper airways.
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| 2. |
- Hjortswang, Henrik, et al.
(författare)
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Infliximab in clinical routine : Experience with Crohn's disease and biomarkers of inflammation over 5 years
- 2009
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Ingår i: European Journal of Gastroenterology and Hepathology. - 0954-691X .- 1473-5687. ; 21:10, s. 1168-1176
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Infliximab was launched for the treatment of Crohn's disease (CD) in 1999. We set up a follow-up protocol to meticulously study disease development with repeated infusions of infliximab. Aim: To follow the effects of infliximab treatment on disease activity, blood chemistry, quality of life, plasma nitrite, and titers of Saccharomyces cerevisiae antibodies (ASCA). Methods: During 1999–2008, CD patients were monitored for disease activity by Harvey–Bradshaw index, blood chemistry with hemoglobin, albumin, C-reactive protein, platelet count, leukocyte count and creatinine, quality of life by the Short Health Scale, and plasma nitrite. During the first year of treatment, follow-up was done repeatedly before and 1 week after each infusion and thereafter every year before the last infusion for 5 years. ASCA was analyzed by flow cytometry with fluorescein isothiocyanate-labelled antibodies. Results: A total of 1061 infusions were given to 103 patients; 92 responders and 11 nonresponders. Responders were further monitored and Harvey–Bradshaw index decreased with infusions during the first year of treatment (P<0.0001), whereas hemoglobin (P<0.01) and albumin (P<0.001) increased, C-reactive protein (P<0.01) decreased, platelets (P<0.001) increased, and leukocytes (P<0.01) decreased. Creatinine was not affected. Short Health Scale (questions analyzed separately) decreased (P<0.0001), and nitrite (P<0.001) increased. During the next 4 years the improved values remained stable. Adverse effects were noted among 32% of the patients; local circulatory reactions being most common. No correlation between ASCA titers and inflammatory activity or infliximab treatment was found. Conclusion: Infliximab treatment is highly effective in responders and maintains symptomatic improvement and low inflammatory activity over years in CD patients.
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| 3. |
- Lindberg, Jenny, et al.
(författare)
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Monocyte and Neutrophil Chemotactic Activity at the Site of Interstitial Inflammation in Patients on High-Flux Hemodialysis or Hemodiafiltration
- 2009
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Ingår i: Blood Purification. - : S. Karger AG. - 0253-5068 .- 1421-9735. ; 28:1, s. 47-52
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: We have observed a difference between patients on low-flux hemodialysis (HD) or peritoneal dialysis and patients on hemodiafiltration (HDF) or high-flux HD in the capacity of transmigrated leukocytes to mobilize CD11b in response to inflammatory stimuli compared with healthy subjects. This could be due to different interstitial chemokine concentrations. Methods: We measured concentrations of circulating and interstitial macrophage inflammatory protein-1 alpha (MIP-1 alpha), matrix metalloproteinase-9 (MMP-9)/neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in 10 patients on HDF or high-flux HD and 11 healthy subjects by using immunoassay. Results: The interstitial concentrations of MIP-1 alpha, MMP-9/NGAL and IL-8 were similar in patients and healthy subjects, while the corresponding concentration of MCP-1 was significantly higher in patients on HDF or high-flux HD as compared with healthy subjects (p < 0.01). Conclusion: We suggest that an equal or higher concentration of chemokines in the interstitium in patients with HDF or high-flux HD might be one mechanism responsible for the preserved function of transmigrated leukocytes. Copyright (C) 2009 S. Karger AG, Basel
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| 4. |
- Nelson, Annika, et al.
(författare)
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Staphylococcus epidermidis Isolated From Newborn Infants Express Pilus-Like Structures and Are Inhibited by the Cathelicidin-Derived Antimicrobial Peptide LL37
- 2009
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Ingår i: Pediatric Research. - 0031-3998 .- 1530-0447. ; 66:2, s. 174-178
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Tidskriftsartikel (refereegranskat)abstract
- Coagulase-negative staphylococci and its subtype Staphylococcus epidermidis are major indigenous Gram-positive inhabitants of the human skin. Colonization occurs in direct connection with birth and terrestrial adaptation. This study focuses on factors that may influence skin colonization of the newborn infant that relates to the immune status of both the bacteria and the host. Skin is an effective barrier against bacteria, and this function is partly mediated by the presence of antimicrobial peptides including human cathelicidin peptide LL37. Grain-positive bacteria have been described to have adhesive pili on their surface that mediates specific attachment to the host. Here, we identify, by negative staining transmission electron microscopy (EM), two different types of pilus-like structures commonly expressed on S. epidermidis isolated from newborn infants. We also show that the cathelicidin antimicrobial peptide LL37, constitutively expressed in the skin barrier of the newborn, significantly inhibited growth of S. epidermidis indicating its importance for the ecological stability of the skin microbiota. Further studies are required to elucidate molecular mechanisms of host-microbe interactions, both for the maintenance of a mutually beneficial homeostatic relationship and for the protection of self when it results in overt disease. (Pediatr Res 66: 174-178, 2009)
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| 5. |
- Paulsson, Josefin, et al.
(författare)
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Activation of peripheral and in vivo transmigrated neutrophils in patients with stable coronary artery disease
- 2007
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Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 192:2, s. 328-334
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Tidskriftsartikel (refereegranskat)abstract
- Accumulating evidence support a role of neutrophils in coronary artery disease (CAD). However little is known about the action of neutrophils at a local inflammatory site represented by an atherosclerotic plaque. To gain insight into these issues, we applied a skin blister model that permits analyses of in vivo transmigrated neutrophils. We hypothesised that the chronic inflammation in stable CAD mediates priming of neutrophils that impacts the out-come of neutrophil action at an inflammatory site. Thirteen patients with angiographically verified CAD were eligible for study entry together with 13 age and sex matched controls. Markers of inflammation (IL-6 and CRP), neutrophil activation (IL-8 and MMP-9/NGAL), and functional aspects (CD11b up-regulation and intracellular H(2)O(2) production) of peripheral and in vivo transmigrated neutrophils were studied. Systemic IL-8 and MMP-9/NGAL concentrations were significantly increased in patients indicating a primed state in circulating neutrophils. In vivo transmigrated neutrophils in stable CAD patients had an increased propensity to release MMP-9/NGAL and a reduced capacity to up-regulate CD11b and to produce hydrogen peroxide. These aberrations at the inflammatory site may be a consequence of a primed state of circulating neutrophils and point towards potential mechanisms whereby neutrophils at a local inflammatory site may contribute to the pathogenesis of CAD.
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| 6. |
- Yektaei-Karin, Elham, et al.
(författare)
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The stress of birth enhances in vitro spontaneous and IL-8-induced neutrophil chemotaxis in the human newborn
- 2007
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Ingår i: Pediatric Allergy and Immunology. - : Wiley. - 0905-6157 .- 1399-3038. ; 18:8, s. 643-651
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Tidskriftsartikel (refereegranskat)abstract
- The birth process induces fetal stress. Stress has profound effects on the immune system, also by acting on the trafficking of leukocytes, a process in which adhesion and chemotaxis are primordial and critical events for the development of effective antimicrobial defenses. The newborn is rapidly challenged by a microflora at the epithelia linings and therefore depending on early, innate immunity onset. The objective of the study was to investigate the immune response in cord blood from newborns in relation to different degrees of fetal stress, with focus on neutrophil chemotaxis. We analyzed in vitro transmigration ability of neutrophils and their CD11b expression, measured total white blood count (WBC) and the major leukocyte populations, interleukin (IL)-8, interferon (IFN)-gamma, and soluble E-Selectin, as well as relevant immuno-modulating hormones in infants born at term after Cesarean section prior to the start of labor (n = 55), normal vaginal delivery (n = 87), and assisted delivery (n = 26). Arterial pH and lactate were used as stress markers. We found that spontaneous and IL-8-induced transmigration ability of neutrophils from newborns after normal delivery was significantly higher compared with that of neutrophils from Cesarean section or from adults. With a progressive increase in fetal stress, there were significant elevations in total WBC, in particular neutrophils and monocytes, as well as an enhanced IL-8 and soluble E-Selectin level. Assisted delivery, associated with the highest degree of fetal stress in addition had an enhanced lymphocyte and monocytes count as well as an increased IFN-gamma level. There were significant direct correlations between neutrophils and monocytes, respectively, with cortisol, beta-endorphin, and prolactin. Interferon-gamma was directly related to dopamine, as well as to the lymphocyte and monocyte count. The setting of the HPA-axis at birth is a promoter of an alarm response and a surge of neuroendocrine immuno-modulating factors that enhances antimicrobial defenses of the newborn. We speculate that IL-8 induced by normal labor may be a priming factor for an increased neutrophil chemotaxis through the pre-activated endothelium of the fetus. Assisted delivery may trigger excessive recruitment of additional inflammatory cells and IFN-gamma release.
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| 7. |
- Zagai, Ulrika, et al.
(författare)
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Eosinophil Cationic Protein Stimulates TGF-β1 Release by Human Lung Fibroblasts In Vitro
- 2007
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Ingår i: Inflammation. - : Springer Science and Business Media LLC. - 0360-3997 .- 1573-2576. ; 30:5, s. 153-160
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Tidskriftsartikel (refereegranskat)abstract
- Eosinophilic inflammation and airway remodeling are features of asthma. Eosinophil cationic protein ( ECP) is released by activated eosinophils and transforming growth factor ( TGF)beta(1) has major functions in the fibrotic process. We therefore hypothesized that ECP stimulates TGF-beta(1) release by human lung fibroblasts. Fibroblasts in monolayer displayed a constitutive release of TGF-beta(1), which increased in presence of ECP ( 436 +/- 60 vs. 365 +/- 48 pg/ ml at 48 h; P< 0.01). mRNA expression of TGF-beta(1) was almost twofold in ECP- stimulated fibroblasts. ECP in threedimensional cultures stimulated both TGF-beta(1) release ( 180 +/- 61 vs. 137 +/- 54 pg/ ml; P< 0.01) and fibroblast- mediated collagen gel contraction ( 28 vs. 39% of initial gel area at 48 h; P< 0.001). ECP stimulates TGF-beta(1) release by human lung fibroblasts, suggesting a potential mechanism for eosinophils in the fibrotic response. This may be an important mechanism by which ECP promotes remodeling of extra cellular matrix leading to airway fibrosis in asthmatics.
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