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表达1型人类免疫缺陷病毒的转基因小鼠中的黏膜念珠菌病

Mucosal candidiasis in transgenic mice expressing human immunodeficiency virus type 1.

作者信息

de Repentigny Louis, Aumont Francine, Ripeau Jean-Sébastien, Fiorillo Marie, Kay Denis G, Hanna Zaher, Jolicoeur Paul

机构信息

Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal and Sainte-Justine Hospital, 3175 Côte-Ste-Catherine, Montreal, Quebec, Canada H3T 1C5.

出版信息

J Infect Dis. 2002 Apr 15;185(8):1103-14. doi: 10.1086/340036. Epub 2002 Mar 21.

DOI:10.1086/340036
PMID:11930320
Abstract

The availability of CD4C/HIV(MutA) transgenic (Tg) mice expressing human immunodeficiency virus type 1 in immune cells and developing an AIDS-like disease has provided the opportunity to devise a model of mucosal candidiasis that closely mimics the clinical and pathologic features of candidal infection in human AIDS. After intraoral infection with Candida albicans, oral burdens were strikingly elevated in the Tg mice, compared with non-Tg littermates (P<.05), during primary infection, a 6-10-week carrier state, and a marked terminal outgrowth preceding death. The chronic carrier state was absent in the non-Tg mice because of clearing of C. albicans. Candida hyphae penetrated the epithelium of the oral cavity, esophagus, and cardial-atrium fold of the stomach, accompanied by a mononuclear cell infiltrate. Immunohistochemical analysis suggested that decreased frequencies of major histocompatibility complex class II-expressing cells, combined with reduced CD4+ cells, may underlie the susceptibility to mucosal candidiasis in these Tg mice.

摘要

在免疫细胞中表达1型人类免疫缺陷病毒并发展出类似艾滋病疾病的CD4C/HIV(MutA)转基因(Tg)小鼠的出现,为设计一种黏膜念珠菌病模型提供了机会,该模型能紧密模拟人类艾滋病中念珠菌感染的临床和病理特征。与非Tg同窝小鼠相比,白色念珠菌经口感染后,Tg小鼠在初次感染、6 - 10周的携带状态以及死亡前明显的终末期增殖阶段,口腔菌量显著升高(P<0.05)。由于白色念珠菌被清除,非Tg小鼠不存在慢性携带状态。念珠菌菌丝穿透口腔、食管和胃贲门-心房皱襞的上皮,伴有单核细胞浸润。免疫组织化学分析表明,主要组织相容性复合体II类表达细胞频率降低,同时CD4+细胞减少,可能是这些Tg小鼠易患黏膜念珠菌病的原因。

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