Investigation of mechanism of acute exacerbation of interstitial pneumonia. Alveolar barrier dysfunction was observed in fibrotic lung

点击翻译按钮获取中文摘要

One of the pathological change of pneumonia, heart failure, and ARDS is thought to be a failure of barrier function of alveolar epithelial cells. We used bleomycin-induced pulmonary fibrosis model. After administration of bleomycin, expressions of tight junction-related proteins, especially claudin-5 and claudin-18 were down-regulated. We also analyzed the influence of transforming growth factor-β (TGF-β), a critical mediator of pulmonary fibrosis on tight junctions in vitro. The addition of TGF-β disrupted expressions of claudins. These results suggest that bleomycin-induced lung injury causes pathogenic alterations in tight junctions and that such alterations seem to be induced by TGF-β.