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弥漫性肺泡损伤中肺泡基底膜的破坏:一项免疫组织化学研究。

Alveolar basement membrane breaks down in diffuse alveolar damage: an immunohistochemical study.

作者信息

Matsubara O, Tamura A, Ohdama S, Mark E J

机构信息

Department of Pathology, School of Medicine, Tokyo Medical and Dental University, Japan.

出版信息

Pathol Int. 1995 Jul;45(7):473-82. doi: 10.1111/j.1440-1827.1995.tb03488.x.

DOI:10.1111/j.1440-1827.1995.tb03488.x
PMID:7551006
Abstract

Sequential structural changes of the alveoli in diffuse alveolar damage (DAD) were examined by immunohistochemical methods. Lung specimens obtained at autopsy from 52 patients with DAD were stained with antibodies to laminin, 7S collagen (7S) and type IV collagen (type IV) for alveolar basement membrane, to von Willebrand factor, CD-31 and thrombomodulin (TM) for the alveolar capillary endothelial cell, and to epithelial membrane antigen and surfactant apo-protein (PE-10) for the alveolar epithelium. Forty-two of the patients had the exudative form of DAD; 10 of the patients had the proliferative form of DAD. The results were summarized as follows: (i) laminin was most easily impaired both in the epithelial and capillary basement membrane in the early exudative stage; (ii) following laminin, 7S and type IV in the capillary basement membrane were also injured in the early exudative stage, and recovered in the proliferative stage; (iii) subsequently, 7S and type IV in the epithelial basement membrane were also impaired in the late exudative stage, and remained impaired even in the proliferative stage; and (iv) alveolar epithelium regenerated almost completely in the late exudative stage, but staining for TM in the alveolar capillary recovered in the proliferative stage. Because the alveolar basement membrane must govern the homeostasis of alveolar tissue architecture, it was concluded that its preservation is necessary to avoid the abnormal remodeling of the alveoli in the reparative stage of DAD, if the patient survives the acute episodes of the disease.

摘要

采用免疫组织化学方法研究了弥漫性肺泡损伤(DAD)中肺泡的系列结构变化。对52例DAD患者尸检获得的肺标本进行染色,使用抗层粘连蛋白、7S胶原蛋白(7S)和IV型胶原蛋白(IV型)抗体检测肺泡基底膜,使用抗血管性血友病因子、CD - 31和血栓调节蛋白(TM)抗体检测肺泡毛细血管内皮细胞,使用抗上皮膜抗原和表面活性蛋白(PE - 10)抗体检测肺泡上皮。其中42例患者为渗出型DAD;10例患者为增殖型DAD。结果总结如下:(i)在渗出早期,上皮和毛细血管基底膜中的层粘连蛋白最易受损;(ii)继层粘连蛋白之后,毛细血管基底膜中的7S和IV型胶原蛋白在渗出早期也受到损伤,并在增殖期恢复;(iii)随后,上皮基底膜中的7S和IV型胶原蛋白在渗出后期也受损,甚至在增殖期仍未恢复;(iv)肺泡上皮在渗出后期几乎完全再生,但肺泡毛细血管中TM的染色在增殖期恢复。由于肺泡基底膜必须维持肺泡组织结构的稳态,因此得出结论,如果患者在疾病急性期存活下来,在DAD修复期避免肺泡异常重塑,保留肺泡基底膜是必要的。

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