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Free Paper Presentation : F-2 ; Interleukin-33 Promotes Production of TGF-b1 in Lung Fibroblast and Neutralization of the IL-33 Ameliorates Bleomycin Induced Experimental Lung Injury/Fibrosis
박성우 , 김초롱 , 고은비 , 장안수 , 김도진 , 박춘식
UCI I410-ECN-0102-2014-500-002059590
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Background: Idiopathic Pulmonary Fibrosis (IPF) is a progressive disease characterized by inappropriate accumulation of fibroblasts and collagen-producing myofibroblasts in lung tissue and no effective therapy has been identified. Recent observations have suggested that IL-33, known Th2 cytokine may contribute progress of IPF. Aims: To investigate the role of IL-33 in the pathogenesis of lung fibrosis and treatment of IL-33 neutralizing antibody have therapeutic effect on bleomycin induced lung injury/fibrosis in mice. Methods: Intranasal or Intraperitoneal treatment of neutralizing IL-33 were performed in bleomycin-treated mouse. Histological examinations, collagen assay and cytokine measurements including IL-1b,IL-13. TNF-a and TGF-β1 were performed. Lung IL-33 expression from the patient with IPF and controls were measured by immunohistochemistry and ELISA. Active form of TGF-b1 levels were measured in IL-13 siRNA knockdown MRC5(fibroblast) cells with or without IL-33 treatment. Results: Compared with control mice, Anti-IL33 treated mice had significantly less lung inflammation, collagen deposition as well as decreased levels of BAL fluid IL-1b,TNF-a and TGF-b1. Lung IL-33 protein expression was significantly increased in patients with IPF than controls. Knock down of IL-13 did not down-regulate IL-33 induced increased levels of active TGF-b1 in MRC-5 cells. Conclusions: Local or systemic treatment of anti-IL33 antibody is effective against the development of experimental lung injury/fibrosis. IL-33 enhances TGF-b1 production in fibroblast IL-13 independent pathway.Background: Idiopathic Pulmonary Fibrosis (IPF) is a progressive disease characterized by inappropriate accumulation of fibroblasts and collagen-producing myofibroblasts in lung tissue and no effective therapy has been identified. Recent observations have suggested that IL-33, known Th2 cytokine may contribute progress of IPF. Aims: To investigate the role of IL-33 in the pathogenesis of lung fibrosis and treatment of IL-33 neutralizing antibody have therapeutic effect on bleomycin induced lung injury/fibrosis in mice. Methods: Intranasal or Intraperitoneal treatment of neutralizing IL-33 were performed in bleomycin-treated mouse. Histological examinations, collagen assay and cytokine measurements including IL-1b,IL-13. TNF-a and TGF-β1 were performed. Lung IL-33 expression from the patient with IPF and controls were measured by immunohistochemistry and ELISA. Active form of TGF-b1 levels were measured in IL-13 siRNA knockdown MRC5(fibroblast) cells with or without IL-33 treatment. Results: Compared with control mice, Anti-IL33 treated mice had significantly less lung inflammation, collagen deposition as well as decreased levels of BAL fluid IL-1b,TNF-a and TGF-b1. Lung IL-33 protein expression was significantly increased in patients with IPF than controls. Knock down of IL-13 did not down-regulate IL-33 induced increased levels of active TGF-b1 in MRC-5 cells. Conclusions: Local or systemic treatment of anti-IL33 antibody is effective against the development of experimental lung injury/fibrosis. IL-33 enhances TGF-b1 production in fibroblast IL-13 independent pathway.

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