Mechanisms of Oncostatin M-Induced Pulmonary Inflammation and Fibrosis
نویسندگان
چکیده
منابع مشابه
Mechanisms of oncostatin M-induced pulmonary inflammation and fibrosis.
Oncostatin M (OSM), an IL-6 family cytokine, has been implicated in a number of biological processes including the induction of inflammation and the modulation of extracellular matrix. In this study, we demonstrate that OSM is up-regulated in the bronchoalveolar lavage fluid of patients with idiopathic pulmonary fibrosis and scleroderma, and investigate the pathological consequences of excess O...
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The development of pulmonary fibrosis is the end point of a wide range of respiratory diseases including organic and inorganic dust exposure, pulmonary infection, acute lung injury, radiation, the idiopathic interstitial pneumonias (IIP), and connective tissue diseases. The most common fibrotic lung disorder is idiopathic pulmonary fibrosis (IPF), an IIP with the histological appearance of usua...
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Mesenchymal stem cells (MSCs) are widely considered for treatment of pulmonary fibrosis based on the anti-inflammatory, antifibrotic, antiapoptotic, and regenerative properties of the cells. Recently, elevated levels of oncostatin M (OSM) have been reported in the bronchoalveolar lavage fluid of a pulmonary fibrosis animal model and in patients. In this work, we aimed to prolong engrafted MSC s...
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متن کاملA mouse model of airway disease: oncostatin M-induced pulmonary eosinophilia, goblet cell hyperplasia, and airway hyperresponsiveness are STAT6 dependent, and interstitial pulmonary fibrosis is STAT6 independent.
Oncostatin M (OSM), a pleiotropic cytokine of the gp130 cytokine family, has been implicated in chronic allergic inflammatory and fibrotic disease states associated with tissue eosinophilia. Mouse (m)OSM induces airway eosinophilic inflammation and interstitial pulmonary fibrosis in vivo and regulates STAT6 activation in vitro. To determine the requirement of STAT6 in OSM-induced effects in viv...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2008
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.181.10.7243