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- Glader, Pernilla, 1975, et al.
(författare)
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Interleukin-17-producing T-helper cells and related cytokines in human airways exposed to endotoxin.
- 2010
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Ingår i: The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology. - : European Respiratory Society (ERS). - 1399-3003. ; 36:5, s. 1155-64
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies on mouse models have indicated that interleukin (IL)-17 and IL-17-producing T-helper (Th) cells are important for pulmonary host defence against Gram-negative bacteria. Human correlates to these findings have not yet been demonstrated. The aim of the present study was to determine whether or not IL-17-producing Th cells are present and whether IL-17 and other Th17-associated cytokines are involved in the immunological response to endotoxin in human airways. Segmental exposure to endotoxin and contralateral exposure to vehicle were performed in the lungs of healthy volunteers, with subsequent bronchoalveolar lavage 12 or 24 h after exposure to study local changes in cytokines and inflammatory cells. Endotoxin exposure increased concentrations of IL-17, IL-22 and their downstream effector molecules, human β-defensin-2 and IL-8/CXC chemokine ligand 8, in bronchoalveolar lavage fluid. Th cells with the capacity to produce IL-17 were found among the bronchoalveolar lavage cells, and expression of IL-17 mRNA correlated with expression of the transcription factor, retinoic-acid-receptor-related orphan receptor C variant 2. Moreover, endotoxin increased the numbers of neutrophils, macrophages and IL-17-producing T-cells, as well as the concentration of the Th17-regulating cytokines, IL-21 and IL-23. In conclusion, IL-17-producing Th cells are present, and IL-17, as well as other Th17-associated cytokines, is involved in the immunological response to endotoxin in human airways.
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| 2. |
- Henningsson, Louise, 1979, et al.
(författare)
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Interleukin-17A during local and systemic Staphylococcus aureus-induced arthritis in mice.
- 2010
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Ingår i: Infection and immunity. - 1098-5522. ; 78:9, s. 3783-90
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Tidskriftsartikel (refereegranskat)abstract
- Staphylococcus aureus is one of the dominant pathogens that induce septic arthritis in immunocompromised hosts, e.g., patients suffering from rheumatoid arthritis treated with immunosuppressive drugs. S. aureus-induced arthritis leads to severe joint destruction and high mortality despite antibiotic treatment. Recently, interleukin-17A (IL-17A) has been discovered to be an important mediator of aseptic arthritis both in mice and humans, but its function in S. aureus-induced arthritis is largely unknown. Here, we investigated the role of IL-17A in host defense against arthritis following systemic and local S. aureus infection in vivo. IL-17A knockout mice and wild-type mice were inoculated systemically (intravenously) or locally (intra-articularly) with S. aureus. During systemic infection, IL-17A knockout mice lost significantly more weight than the wild-type mice did, but no differences were found in the mortality rate. The absence of IL-17A had no impact on clinical arthritis development but led to increased histopathological erosivity late during systemic S. aureus infection. Bacterial clearance in kidneys was increased in IL-17A knockout mice compared to the level in wild-type mice only 1 day after bacterial inoculation. During systemic S. aureus infection, serum IL-17F protein levels and mRNA levels in the lymph nodes were elevated in the IL-17A knockout mice compared to the level in wild-type mice. In contrast to systemic infection, the IL-17A knockout mice had increased synovitis and erosions and locally decreased clearance of bacteria 3 days after local bacterial inoculation. On the basis of these findings, we suggest that IL-17A is more important in local host defense than in systemic host defense against S. aureus-induced arthritis.
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| 3. |
- Lindén, Anders, 1961, et al.
(författare)
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Airways remodelling in asthma Preface
- 2010
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Ingår i: Preface. Clinical Respiratory Journal 2010. ; 44 Suppl 1, s. III-III
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 4. |
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| 6. |
- Olsson, Lars E, et al.
(författare)
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1H and hyperpolarized 3He magnetic resonance imaging clearly detect the preventative effect of a glucocorticoid on endotoxin-induced pulmonary inflammation in vivo.
- 2010
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Ingår i: Innate immunity. - : SAGE Publications. - 1753-4267 .- 1753-4259. ; :Feb 3
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Proton ((1)H) magnetic resonance imaging (MRI) can be utilized to quantify pulmonary edema in endotoxin-induced pulmonary inflammation and hyperpolarized (HP) (3)He MRI can assess pulmonary ventilation. Neither of the methods has been applied to assess the impact of a drug on endotoxin-induced pulmonary inflammation in vivo. The aim of the current study was to evaluate the capability of (1)H and HP (3)He MRI to assess the effects of a glucocorticoid on endotoxin-induced pulmonary inflammation in vivo.Materials and Methods: Mice were exposed to an aerosol of either saline or endotoxin (5 mg/ml) for 10 min. Half of the endotoxin-exposed mice were pretreated with a glucocorticoid (budesonide 3 mg/kg; 2 times/day) and the other half with vehicle p.o. The first budesonide treatment was administered 1 h prior to the aerosol inhalation. Forty-eight hours after the aerosol exposure, the mice were anaesthetized for subsequent imaging. Hyperpolarized (3)He was administered and axial MR images of the lungs obtained. Matching (1)H MR images were then acquired. The mice were sacrificed and broncho-alveolar lavage (BAL) samples were harvested to determine total and cell differential counts.Results: The lesion volume on both (1)H and (3)He MRI, were markedly increased by endotoxin exposure (P < 0.001). Budesonide strongly reduced lesion volume (P < 0.001). The BAL cell count correlated strongly with both (3)He (P < 0.001; r = 0.96) and (1)H lesion volumes (P < 0.001; r = 0.97).Conclusions: Hyperpolarized (3)He MRI and (1)H MRI clearly visualized the preventative effect of budesonide on the impact of endotoxin on pulmonary ventilation and edema, respectively. The fact that ventilation defects on (3)He MRI corresponded to findings from conventional (1)H MRI, as well as to counts of BAL inflammatory cells suggests that these imaging techniques constitute promising tools for non-invasive monitoring of pulmonary inflammation in vivo.
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| 7. |
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| 8. |
- Riise, Gerdt C., 1956, et al.
(författare)
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Increased net gelatinase but not serine protease activity in bronchiolitis obliterans syndrome.
- 2010
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Ingår i: 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
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Tidskriftsartikel (refereegranskat)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.
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| 9. |
- Vlahos, Ross, et al.
(författare)
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Neutralizing granulocyte/macrophage colony-stimulating factor inhibits cigarette smoke-induced lung inflammation.
- 2010
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Ingår i: American journal of respiratory and critical care medicine. - 1535-4970. ; 182:1, s. 34-40
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Tidskriftsartikel (refereegranskat)abstract
- Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), and there is currently no satisfactory therapy to treat people with COPD. We have previously shown that granulocyte/macrophage colony-stimulating factor (GM-CSF) regulates lung innate immunity to LPS through Akt/Erk activation of nuclear factor-kappaB and activator protein (AP)-1.
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