The study of molecular mechanism and new therapeutic strategy for the pathogenesis of inflammatory pulmonary di sease

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To put the molecular mechanism for pathogenesis of inflammatory pulmonary diseases to practical use, the following studies were performed. (1) Focusing on p38 which plays a central role in various inflammatory responses, one of mitogen-activated protein kinase (MAPK), we tried to produce transgenic mice exhibiting p38 activation in tetracycline-dependent and site (type II alveolar epithelial cell: AECII)-specific manners. (2) We confirmed that severity of bleomycin-induced interstitial pneumonia/pulmonary fibrosis is clearly dependent on the degree of p38 activation in AECII and that IL-6 produced from AECII plays a crucial role in the pathogenesis as a trigger. (3) We induced chronic obstructive pulmonary disease (COPD) in mice and comprehensively estimated plausible candidate molecules in COPD.