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[氯化汞诱导的大鼠肠病:一种具有免疫发病机制的胃肠疾病模型]

[Mercuric chloride-induced enteropathy in the rat: a model of gastrointestinal disease with immunologic pathogenesis].

作者信息

Knoflach P, Albini B

机构信息

II. Universitätsklinik für Gastroenterologie und Hepatologie Wien.

出版信息

Acta Med Austriaca. 1987;14(5):107-11.

PMID:2964159
Abstract

Protein-loss into the gastrointestinal tract is a feature of many different diseases, a number of which are immunologically mediated, e.g. systemic lupus erythematosus or Crohn's disease. The pathogenic mechanism of protein-losing enteropathy in diseases without obvious enterocyte injury are unknown. Brown-Norway-rats (BN-rats) were gavaged with low doses of HgCl2 for 39 weeks. Within 2 weeks, the intestines showed strong linear staining for IgG and IgA along vascular and intestinal basement membranes. Granular deposits containing IgG and C3 were present along intestinal basement membrane only in the late stages of the experiment; only in these animals increased intestinal protein loss as measured by fecal Cr-51 excretion was found. These findings suggest that immune complex deposition along the intestinal basement membrane can lead to protein-losing enteropathy. This disease may be used as a model for the study of immunologically mediated intestinal disease.

摘要

蛋白质丢失到胃肠道是许多不同疾病的一个特征,其中一些疾病是由免疫介导的,例如系统性红斑狼疮或克罗恩病。在没有明显肠上皮细胞损伤的疾病中,蛋白质丢失性肠病的致病机制尚不清楚。给棕色挪威大鼠(BN大鼠)灌胃低剂量的HgCl2,持续39周。在2周内,肠道沿血管和肠基底膜显示出强烈的IgG和IgA线性染色。仅在实验后期,沿肠基底膜出现了含有IgG和C3的颗粒沉积物;仅在这些动物中,通过粪便Cr-51排泄量测定发现肠道蛋白质丢失增加。这些发现表明,沿肠基底膜的免疫复合物沉积可导致蛋白质丢失性肠病。这种疾病可作为研究免疫介导的肠道疾病的模型。

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