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布氏布氏锥虫诱导小鼠心脏病的模型。组织学和免疫病理学研究。

A model for cardiopathy induced by Trypanosoma brucei brucei in mice. A histologic and immunopathologic study.

作者信息

Poltera A A, Hochmann A, Lambert P H

出版信息

Am J Pathol. 1980 May;99(2):325-52.

PMID:6990771
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1903500/
Abstract

The successful induction of pancarditis in mice by the use of Trypanosoma brucei brucei is reported. The sequential analysis of whole-organ sections demonstrated the presence of trypanosomes in the cardiac structures from the fourth week after infection. Parasites predominated on the endocardial and epicardial side but were also present in the valves, the conducting system, and the lymphatic system draining the heart, the latter being particularly evident in late infection. At the time of parasite invasion, deposits of IgM and IgG and of complement (C3) appeared in the tissues. Also at this time parasitemia reached a plateau, and the circulating specific antitrypanosomal antibodies, the serum Ig and C3, as well as the Clq activity, reached pathologic levels. Cellular response followed parasite invasion and appeared to be similar to that described in human African trypanosomiasis. In late infection, the draining lymph nodes showed a marked histiocytic proliferation, and the vessels became convoluted and distended. The suggested pathogenic mechanisms involve immunologic and mechanical factors. It is possible that the immunologic process prepares for a simultaneous or subsequent parasite invasion of the tissues with an associated inflammatory response. The partial obstruction of the lymphatic cardiac draining system probably accounts at least in part for the peculiar distribution of the parasite-induced lesions. A therapeutic trial was unsuccessful, but the persistence of trypanosomes in the tissues when circulating parasites were no longer detectable may account for relapses.

摘要

据报道,利用布氏布氏锥虫成功诱导小鼠发生全心炎。对全器官切片的序贯分析表明,感染后第四周心脏结构中存在锥虫。寄生虫主要存在于心内膜和心外膜侧,但也存在于瓣膜、传导系统以及引流心脏的淋巴系统中,后者在感染后期尤为明显。在寄生虫侵入时,组织中出现了IgM、IgG和补体(C3)沉积。此时寄生虫血症也达到平台期,循环中的特异性抗锥虫抗体、血清Ig和C3以及Clq活性均达到病理水平。细胞反应在寄生虫侵入后出现,似乎与人类非洲锥虫病中描述的情况相似。在感染后期,引流淋巴结出现明显的组织细胞增生,血管变得迂曲和扩张。推测的致病机制涉及免疫和机械因素。免疫过程可能为寄生虫同时或随后侵入组织并伴有炎症反应做好了准备。心脏淋巴引流系统的部分阻塞可能至少部分解释了寄生虫诱导病变的特殊分布。一项治疗试验未获成功,但当循环中的寄生虫不再可检测到时,组织中锥虫的持续存在可能是复发的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/74fdb5bcdcce/amjpathol00231-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/c2c8ff32848e/amjpathol00231-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/5ca072ebbc01/amjpathol00231-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/43262e5480f5/amjpathol00231-0101-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/4ea34ca6ed39/amjpathol00231-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/93e130eeafe6/amjpathol00231-0103-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/74fdb5bcdcce/amjpathol00231-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/c2c8ff32848e/amjpathol00231-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/5ca072ebbc01/amjpathol00231-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/43262e5480f5/amjpathol00231-0101-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/4ea34ca6ed39/amjpathol00231-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/93e130eeafe6/amjpathol00231-0103-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806c/1903500/74fdb5bcdcce/amjpathol00231-0095-a.jpg

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