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目的探讨严重急性呼吸综合征(SARS)肺组织急性损伤后发生肺纤维化及其发病机制。方法应用免疫组织化学染色方法,检测4例不同病程和病变的SARS肺组织和2例正常肺组织的细胞外基质(FN,LN,ColⅠ,ColⅣ)及间质效应细胞骨架蛋白表型(Des,Vim,HHF-35,SMA)的变化。结果FN在SARS肺组织急性渗出期大量出现,并逐渐增强至纤维增殖期,而在胶原硬化期明显减弱,LN仅在纤维增殖期呈强阳性,急性渗出期和胶原硬化期阳性信号弱,ColⅠ及ColⅣ在急性渗出期近乎看不见,而在纤维增殖期和胶原硬化期逐渐增强,以ColⅣ为主。Des,Vim,HHF-35和SMA从急性渗出期向纤维增殖期增强的趋势,在胶原硬化期逐渐减弱,以HHF-35和Des减弱直至消失。结论SARS肺组织纤维化是细胞外基质过多积聚的结果,原始间叶细胞的增生和分化是肺纤维化的重要因素。
Objective To investigate the pathogenesis of pulmonary fibrosis after acute lung injury in severe acute respiratory syndrome (SARS). Methods The expression of extracellular matrix (FN, LN, ColⅠ, ColⅣ) and the stromal protein of stromal cells in four kinds of SARS lung tissues and two normal lung tissues were detected by immunohistochemical staining. Vim, HHF-35, SMA). Results FN was found in acute exacerbation stage of SARS and gradually increased to fibroblast stage. However, FN decreased significantly during the period of collagen sclerosis. LN was only strongly positive in fibroblasts stage, weak in acute stage of exudative stage and in collagen sclerosis stage Col I and Col IV were almost invisible during acute exudation, but gradually increased during fibrosis and collagen sclerosis. The trend of Des, Vim, HHF-35 and SMA increasing from acute exudative period to fibroblast proliferation was gradually weakened during collagen sclerosis, and weakened and disappeared with HHF-35 and Des. Conclusions Lung fibrosis in SARS is the result of excessive accumulation of extracellular matrix. Proliferation and differentiation of primitive mesenchyme cells are important factors of pulmonary fibrosis.