Type ¢ò Alveolar Epithelial Cells In Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is characterized by diffusefibrosis and remodelling of the architecture of pulmonary parenchymawith unknown origin. Development of lesions is preceded by aninflammatory response, often dominated by local infiltration ofmacrophages and lymphocytes, the mechanism of which is not clear. Ourpurpose of this research was to investigate the influence of pulmonarytype II epithelial cells on the inflammatory process of EPF. In thisresearch, we observed the expression of monocyte chemotactic protein (MCP) -1 mRNA in pulmonary type II epithelial cells stimulated bybleomycin, alveolar macrophage-conditioned media (AMCM) and bleomycintreated alveolar macrophage-conditioned media (BMCM) respectively. Toget a better understanding about the infiltration of macrophages inlungs, the supernatants of pulmonary type II epithelial cells culturedin different conditions above were collected and monocyte chemotacticeffect of the supernatants observed. There was MCP-1 mRNA expression inunstimulated pulmonary type II cells, and the expression were 46%, 260%, and 307% higher after stimulated by bleomycin, AMCM, and BMCMcorrespondly. Monocyte chemotactic effect of supernatants ofunstimulated pulmonary type epithelial cells was also found and theeffect were 60%, 143%, and 232% higher after stimulated by bleomycin,AMCM, and BMCM correspondly. The results demonstrated that pulmonarytype II epithelial cells participated in the regulation of inflammatoryprocess of IPF. A network of cytokines was formed between pulmonarytype II epithelial cells and alveolar macrophages, in which theepithelial cells effected as an inflammatory enhancer.