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首页> 外文期刊>Infection and immunity >Macrophage-Mediated Responses to Candida albicans in Mice Expressing the Human Immunodeficiency Virus Type 1 Transgene
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Macrophage-Mediated Responses to Candida albicans in Mice Expressing the Human Immunodeficiency Virus Type 1 Transgene

机译：巨噬细胞介导的白色念珠菌在表达人类免疫缺陷病毒1型转基因小鼠中的反应。

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The critical impairments of innate and adaptive immunity that cause susceptibility to mucosal candidiasis in human immunodeficiency virus (HIV) infection have not been fully determined. We therefore conducted an analysis of macrophage-mediated responses to Candida albicans in transgenic (Tg) mice expressing Nef, Env, and Rev of HIV type 1 (HIV-1) in CD4+ T cells, dendritic cells, and macrophages and developing an AIDS-like disease (CD4C/HIVMutA Tg mice). Macrophages were successfully recruited to the oral and gastric mucosae of these Tg mice in response to chronic carriage of C. albicans and displayed polarization toward an alternatively activated phenotype. Functionally, peritoneal macrophages from uninfected Tg mice exhibited increased phagocytosis of C. albicans and enhanced production of interleukin 6 and monocyte chemoattractant protein 1, demonstrating that the HIV-1 transgene independently activates selected macrophage functions. Production of H2O2 by macrophages from Tg mice primed with gamma interferon and treated with phorbol 12-myristate 13-acetate or C. albicans was moderately reduced, but expression of the HIV-1 transgene did not alter production of nitric oxide or reduce killing of C. albicans. A knockout of the inducible nitric oxide synthase (NOS2) gene in these Tg mice did not augment oral or gastrointestinal burdens during chronic carriage of C. albicans or cause systemic dissemination, likely due to a redundancy provided by partially preserved production of H2O2 and oxygen-independent candidacidal mechanisms. Thus, the macrophage response to C. albicans is largely preserved in these Tg mice, and no functional macrophage defect appears to primarily determine the susceptibility to mucosal candidiasis.
机译：尚未完全确定导致人类免疫缺陷病毒（HIV）感染易感粘膜念珠菌的先天性和适应性免疫的严重损害。因此，我们进行了在CD4 + 中表达Nef，Env和HIV 1型HIV（HIV-1）Rev的转基因（Tg）小鼠中巨噬细胞介导的对白色念珠菌的反应。 sup> T细胞，树突状细胞和巨噬细胞，并发展为AIDS样疾病（CD4C / HIV MutA Tg小鼠）。巨噬细胞被成功招募到这些Tg小鼠的口腔和胃粘膜，以响应慢性携带 C。白色念珠，并向交替激活的表型显示极化。从功能上讲，来自未感染的Tg小鼠的腹膜巨噬细胞表现出增加的 C吞噬作用。并增强白细胞介素6和单核细胞趋化蛋白1的产生，表明HIV-1转基因独立激活选定的巨噬细胞功能。巨噬细胞产生的H 2 O 2 是由Tg小鼠经γ-干扰素引发并经佛波醇12-肉豆蔻酸酯13-乙酸酯或 C处理后产生的。 Albicans 适度降低，但HIV-1转基因的表达不会改变一氧化氮的产生或减少 C的杀死。白色的。在这些Tg小鼠中，可诱导型一氧化氮合酶（NOS2）基因的敲除并没有增加C的长期运输过程中的口服或胃肠道负担。白色念珠菌或引起全身性传播，可能是由于部分保存的H 2 O 2 产生的冗余和不依赖氧的候选酸机制所致。因此，巨噬细胞对 C的反应。在这些Tg小鼠中大部分保留了白色念珠菌，并且似乎没有功能性巨噬细胞缺陷主要决定对粘膜念珠菌病的易感性。

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