人肺泡包虫病肝纤维化的胶原免疫分型研究。

D A Vuitton, S Guerret-Stocker, J P Carbillet, G Mantion, J P Miguet, J A Grimaud
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引用次数: 35

摘要

肺泡棘球蚴病(AE)是一种严重的寄生虫病,是由多房棘球蚴的幼虫在肝脏中发育引起的。对9例AE患者肝脏纤维区、肉芽肿区和正常区胶原进行免疫分型。胶原类型的免疫荧光标记显示,致密纤维化完全由I型和III型胶原的粗束组成,其周围有一层自荧光层压层围绕着老的寄生囊泡。在肉芽肿区,胶原被标记为主要由III型前胶原和胶原组成的簇。III型胶原的同心束围绕着活跃的寄生囊泡。在所有患者中,完整肝脏门静脉间隙的正常标记增强。这些结果表明,AE中观察到的不可逆的脱细胞瘢痕样纤维化是与宿主免疫应答相关的细胞毒性和纤维发生事件的最终结果,这些事件最初发生在寄生虫幼体周围的肉芽肿区域。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Collagen immunotyping of the hepatic fibrosis in human alveolar echinococcosis.

An extremely dense fibrosis is responsible for the main complications of alveolar echinococcosis (AE), a severe parasitic disease due to the development in the liver of a larval form of the cestode Echinococcus multilocularis. Immunotyping of collagens present in fibrous, granulomatous, and normal areas of the liver was performed in nine patients with AE. Immunofluorescent labelling of collagen types showed that dense fibrosis was entirely composed of thick bundles of type I and type III collagens, surrounding old parasitic vesicles with an autofluorescent laminated layer. In granulomatous areas, collagens were labelled as clusters consisting mainly of type III procollagen and collagen. Concentric bundles of type III collagen surrounded active parasitic vesicles. An enhancement of the normal labelling in portal spaces of the intact liver was present in all the patients. These results suggest that irreversible acellular keloid scar-like fibrosis observed in AE is the ultimate result of cytotoxic and fibrogenetic events related to the immune response of the host which are taking place initially in the granulomatous area surrounding the young parasite larvae.

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