Kennedy M J, Volz P A, Edwards C A, Yancey R J
Microbiology and Nutrition Research Unit, Upjohn Company, Kalamazoo, Michigan 49001.
J Med Microbiol. 1987 Dec;24(4):333-41. doi: 10.1099/00222615-24-4-333.
The association of Candida albicans with gastrointestinal (GI) mucosal surfaces was studied in vitro and in vivo. The caecal mucosal surfaces from antibiotic-treated and untreated control mice challenged orally with C. albicans revealed that large numbers of C. albicans were associated with the intestinal epithelium of antibiotic-treated mice but not with that of the control mice that possessed an indigenous wall-associated bacterial flora. Moreover, Candida cells only penetrated deep into the mucosa of animals in which the ecology of the intestinal microflora had been disrupted. In mice given antibiotics, C. albicans was associated with the mucosa of all areas of the GI tract; the caecal mucosa had the most associated Candida, whereas the stomach and small intestine had very few associated yeasts. Further examination of caecal mucosa from antibiotic-treated mice showed that C. albicans associated with the mucosa by at least five distinct mechanisms. These included: adhesion to epithelium, adhesion to mucus, co-adhesion to adherent fungi, co-adhesion to adherent bacteria, and entrapment in the mucous gel overlying the epithelium. The cell-surface hydrophobicity of C. albicans also was examined and found not to play a role in Candida adhesion to intestinal mucosa. The predominant association mechanisms appeared to be entrapment in the mucous gel, and adhesion to mucus and the epithelium. The ecological and pathological significance of co-adhesion by C. albicans to attached organisms is unclear but it may be important in the initiation of mucosal lesions.
对白色念珠菌与胃肠道(GI)黏膜表面的关联进行了体外和体内研究。用白色念珠菌经口攻击抗生素处理组和未处理的对照小鼠后,对其盲肠黏膜表面进行观察,结果显示,大量白色念珠菌与抗生素处理组小鼠的肠上皮细胞相关联,而与拥有固有壁相关细菌菌群的对照组小鼠的肠上皮细胞无关联。此外,念珠菌细胞仅深入到肠道微生物群落生态遭到破坏的动物的黏膜中。在给予抗生素的小鼠中,白色念珠菌与胃肠道所有区域的黏膜相关联;盲肠黏膜表面的念珠菌数量最多,而胃和小肠中的相关酵母菌数量很少。对经抗生素处理的小鼠的盲肠黏膜进行进一步检查发现,白色念珠菌与黏膜的关联至少通过五种不同机制。这些机制包括:黏附于上皮细胞、黏附于黏液、与黏附真菌共同黏附、与黏附细菌共同黏附以及被困于覆盖上皮细胞的黏液凝胶中。还对白色念珠菌的细胞表面疏水性进行了检测,发现其在念珠菌对肠黏膜的黏附中不起作用。主要的关联机制似乎是被困于黏液凝胶中,以及黏附于黏液和上皮细胞。白色念珠菌与附着生物共同黏附的生态和病理意义尚不清楚,但可能在黏膜病变的起始过程中起重要作用。