Bronchiolar and alveolar epithelial cell apoptosis in pulmonary fibrosis

肺纤维化是由成纤维细胞增殖的组织重塑引起的，由细支气管和肺泡上皮细胞损伤和炎症延长所致。我们验证了炎症细胞和肺上皮细胞的凋亡可能参与这一过程的假说。我们在下面描述了该摘要。1)IPF患者肺上皮细胞DNA损伤和P53、p21的过度表达；2)IPF患者肺上皮细胞Fas和FasL表达上调；3)博莱霉素性肺炎肺上皮细胞中P53、Fas、FasL表达上调；4)吸入激动型抗Fas抗体诱导的肺纤维化；5)Fas或FasL缺陷小鼠对博莱霉素性肺损伤具有抵抗力；6)caspase抑制剂减轻脂多糖或博莱霉素性肺损伤。

Pulmonary fibrosis caused by tissue remodeling consisting of fibroblast proliferation, which is induced by bronchiolar and alveolar epithelial cell damage and prolongation of inflammation. We have examined the hypothesis that apoptosis of inflammatory cells and lung epithelial cells may be involved in this process. We described the abstract below. 1) DNA damage and p53 and p21 overexpression in lung epithelial cells from patients with IPF 2) Fas and FasL upregulation in lung epithelial cells and infiltrating lymphocytes, respectively, in lung epithelial cells from patients with IPF 3) Upregulation of p53, Fas, FasL in bleomycin-induced pneumopathy 4) Pulmonary fibrosis induced by inhalation of agonistic anti-Fas antibody 5) Fas- or FasL-deficient mice are resistant against bleomycin-induced pneumopathy 6) Amelioration of LPS- or bleomycin induced pneumopathy in mice by a caspase inhibitorThese results suggest that lung epithelial cell apoptosis is involved in the pathophysiology of pulmonary fibrosis.