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摄入氯化汞的棕色挪威大鼠肠道中的IgA-IgG疾病

IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric chloride.

作者信息

Andres P

出版信息

Clin Immunol Immunopathol. 1984 Mar;30(3):488-94. doi: 10.1016/0090-1229(84)90034-5.

Abstract

In Brown-Norway (BN) rats, oral administration of mercuric chloride (HgCl2) induced morphological lesions of the ileum and, in lesser degree, of the colon, with abnormal deposits of IgA in the basement membranes of intestinal glands and of IgG in the basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and with the lamina propria of a normal BN rat was found in the serum and IgG deposits were present in renal glomeruli of BN rats receiving HgCl2. Thus, it is conceivable that the deposits of IgG present in the intestine resulted from local fixation of circulating autoantibodies. In contrast, IgA with basement membrane reactivity was not detected in the sera nor in the renal glomeruli, suggesting that the intestinal deposits of IgA were formed in situ. This IgA-IgG intestinal disease inducible in BN rats may provide a model for the study of alterations of the secretory IgA system, as well as for testing the possibility that abnormal deposits IgA-IgG in the intestinal structures are associated with local functional changes.

摘要

在布朗-挪威(BN)大鼠中,口服氯化汞(HgCl2)会导致回肠出现形态学损伤,结肠损伤程度较轻,肠道腺体基底膜中有IgA异常沉积,基底膜和固有层中有IgG异常沉积。血清中发现了与正常BN大鼠肾和肠基底膜以及固有层发生反应的IgG,接受HgCl2的BN大鼠的肾小球中也存在IgG沉积。因此,可以推测肠道中存在的IgG沉积是循环自身抗体局部固定的结果。相比之下,血清和肾小球中均未检测到与基底膜发生反应的IgA,这表明肠道中的IgA沉积是原位形成的。这种在BN大鼠中可诱导的IgA-IgG肠道疾病可能为研究分泌性IgA系统的改变提供一个模型,也为测试肠道结构中异常的IgA-IgG沉积是否与局部功能变化相关的可能性提供一个模型。

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