Cole G T, Saha K, Seshan K R, Lynn K T, Franco M, Wong P K
Department of Botany, University of Texas, Austin 78713-7640.
Infect Immun. 1992 Oct;60(10):4168-78. doi: 10.1128/iai.60.10.4168-4178.1992.
Dysfunction of neutrophils in patients infected with human immunodeficiency virus is at least partly responsible for secondary microbial diseases in these individuals, including invasive gastrointestinal (GI) candidiasis. Immunoregulatory disturbances associated with the development of AIDS in human immunodeficiency virus-infected patients exacerbates Candida albicans infection of the upper GI tract and frequently leads to oropharyngeal and esophageal candidiasis. In this article, we present the first report of a murine model of invasive GI candidiasis associated with an AIDS-related murine immunodeficiency syndrome that results from infection of C57BL/6 mice with a previously described retrovirus complex (LP-BM5). Mice of the inbred strain were infected with C. albicans by oral-intragastric inoculation as infants and with the retrovirus by the intraperitoneal route 30 days later. Control mice of the same strain were infected with C. albicans as above and subsequently infected with the avirulent, ecotropic helper virus (MBI-5). Animals were killed 90 days after retroviral challenge. Total and differential blood cell counts, CD4+ T-cell counts in the spleen, and the histopathology of the gastric mucosa of experimental and control animals were determined. The virulent LP-BM5-infected animals developed murine AIDS and showed eruptive and suppurative lesions, with associated C. albicans mainly in regions of the cardial-atrium fold of the stomach. Well-defined abscesses with entrapped C. albicans hyphae were observed in the region of the cardial-atrium fold of control mice. A significant increase in the number of C. albicans CFU in homogenized and plated segments of the GI tract was recognized in mice with murine AIDS versus the control animals. The murine model of GI candidiasis reported here permits examination of the nature of C. albicans interaction with the gastric mucosa both in the immunocompetent host under conditions in which the yeast exists predominantly as a commensal organism and in the immunosuppressed host during progressive stages of AIDS induced by a retroviral infection.
感染人类免疫缺陷病毒（HIV）的患者中性粒细胞功能障碍至少部分导致了这些个体的继发性微生物疾病，包括侵袭性胃肠道（GI）念珠菌病。与人类免疫缺陷病毒感染患者艾滋病发展相关的免疫调节紊乱会加剧白色念珠菌对上消化道的感染，并经常导致口咽和食管念珠菌病。在本文中，我们首次报告了一种与艾滋病相关的小鼠免疫缺陷综合征相关的侵袭性胃肠道念珠菌病小鼠模型，该模型由C57BL/6小鼠感染先前描述的逆转录病毒复合物（LP-BM5）所致。近交系小鼠在幼年时通过口服胃内接种感染白色念珠菌，30天后通过腹腔途径感染逆转录病毒。相同品系的对照小鼠按上述方法感染白色念珠菌，随后感染无毒的嗜亲性辅助病毒（MBI-5）。在逆转录病毒攻击90天后处死动物。测定实验动物和对照动物的全血细胞计数和分类计数、脾脏中CD4+T细胞计数以及胃黏膜的组织病理学。感染毒性LP-BM5的动物发展为小鼠艾滋病，并出现皮疹和化脓性病变，相关白色念珠菌主要存在于胃的心-心房皱襞区域。在对照小鼠的心-心房皱襞区域观察到有白色念珠菌菌丝被困的明确脓肿。与对照动物相比，患有小鼠艾滋病的小鼠胃肠道匀浆和接种平板部分中的白色念珠菌CFU数量显著增加。本文报道的胃肠道念珠菌病小鼠模型允许在酵母主要作为共生生物存在的免疫活性宿主以及逆转录病毒感染诱导的艾滋病进展阶段的免疫抑制宿主中，研究白色念珠菌与胃黏膜相互作用的性质。
