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首页> 外文期刊>Infection and immunity >Oral carriage of Candida albicans in murine AIDS.
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Oral carriage of Candida albicans in murine AIDS.

机译：在小鼠艾滋病中口服白色念珠菌。

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Oral candidiasis is a common fungal infection in patients infected with the human immunodeficiency virus (HIV). Although rare at the time of primary HIV infection, it is frequently found throughout the asymptomatic phase and is predictive of progressive immunodeficiency. However, the precise immune defect which results in outgrowth of commensal Candida albicans in HIV infection has not been identified. Mice infected with the Du5H(G6T2) mixture of mouse leukemia viruses develop a syndrome, designated murine AIDS (MAIDS), that has many of the immune abnormalities found in HIV infection. Retrovirus-infected C57BL/6 mice were examined for their ability to resist the development of oral candidiasis from the carrier state established after a self-limiting acute infection and to clear a subsequent secondary inoculum of oral C. albicans. Most of the mice orally colonized with C. albicans and then inoculated with the retrovirus mixture maintained a low-level oral carriage of C. albicans, while 30% of coinfected mice developed recurring 2- to 3-week episodes of acute Candida proliferation, separated by transient recoveries to the carrier state. The frequencies of CD4+ and CD8+ lymphocytes were, respectively, unchanged and significantly decreased (P < 0.05) in both cervical lymph nodes and spleens of coinfected mice compared to the corresponding frequencies in C. albicans-carrying, virus-free, age-matched control animals. Secretion of gamma interferon by concanavalin A (ConA)-stimulated spleen cells from Candida-carrying, retrovirus-infected mice was significantly decreased (P < 0.05) compared to that of C. albicans-carrying, retrovirus-free mice, in accordance with known abnormalities associated with MAIDS. However, production of this cytokine by ConA-stimulated or unstimulated cervical lymph node cells from coinfected mice was enhanced compared to that of virus-free animals colonized with C. albicans. Acquired resistance to reinfection with C. albicans was maintained in retrovirus-infected mice and was associated with a mucosal recruitment of CD8+ cells not observed in control mice. These results suggest that alterations in mucosal immunity which occur in MAIDS differ substantially from defects observed at other sites and that surrogate epithelial defense mechanisms may function locally to limit Candida proliferation.
机译：念珠菌病是感染人类免疫缺陷病毒（HIV）的患者的常见真菌感染。尽管在原发性HIV感染时很少见，但在无症状阶段经常发现，可预示进行性免疫缺陷。但是，尚未发现导致白化念珠菌在HIV感染中生长过度的确切免疫缺陷。感染了小鼠白血病病毒Du5H（G6T2）混合物的小鼠会产生一种称为鼠类艾滋病（MAIDS）的综合征，该综合征具有HIV感染中发现的许多免疫异常。检查了逆转录病毒感染的C57BL / 6小鼠抵抗自限性急性感染后建立的携带者状态抵抗口腔念珠菌病发展的能力，并清除了随后的口腔念珠菌继发接种物。大部分口服白色念珠菌定植然后用逆转录病毒混合物接种的小鼠维持了白色念珠菌的低水平口服运输，而30％的并发感染小鼠出现了2-3周急性念珠菌增殖的发作，分离了通过短暂恢复到载流子状态。与携带白色念珠菌的，无病毒的，年龄匹配的对照组中的相应频率相比，共感染小鼠的颈部淋巴结和脾脏中的CD4 +和CD8 +淋巴细胞的频率分别保持不变并显着降低（P <0.05）动物。与携带白色念珠菌的无逆转录病毒的小鼠相比，伴有念珠菌的逆转录病毒感染的小鼠经伴刀豆球蛋白A（ConA）刺激的脾细胞分泌的γ干扰素明显减少（P <0.05）。与MAIDS相关的异常。但是，与定植在白色念珠菌中的无病毒动物相比，用ConA刺激或未刺激的宫颈癌淋巴结细胞从共感染小鼠中产生的这种细胞因子得到了增强。在逆转录病毒感染的小鼠中保持了对白色念珠菌再感染的抗性，并且与在对照小鼠中未观察到的CD8 +细胞的粘膜募集有关。这些结果表明，在MAIDS中发生的粘膜免疫改变与在其他部位观察到的缺陷大不相同，替代性上皮防御机制可能在局部发挥作用，限制念珠菌的增殖。

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