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首页> 外文期刊>Infection and immunity >Scanning electron microscopy of epidermal adherence and cavitation in murine candidiasis: a role for Candida acid proteinase.
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Scanning electron microscopy of epidermal adherence and cavitation in murine candidiasis: a role for Candida acid proteinase.

机译：小鼠念珠菌病中表皮粘附和空化的扫描电子显微镜：念珠菌酸蛋白酶的作用。

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Adherence of blastoconidia to epidermal corneocytes is an early event in Candida colonization and infection of the skin. Pathogenic species adhere more avidly than nonpathogenic species, transform to hyphal growth, and invade the stratum corneum of the skin. Adherence was studied by scanning electron microscopy of experimental murine cutaneous Candida infections, using six species of Candida. Candida albicans and C. stellatoidea blastoconidia, applied to newborn mouse skin, adhered to the stratum corneum in greater numbers than other species tested, acquired fibrils and strands of amorphous mucinlike material ("cohesin") between spores and the corneocyte cell surface, formed cavitations in the corneocyte surface, and invaded the corneocyte envelope by hyphal growth at sites distant to the point of blastoconidia attachment. Other species showed little or no adherence, colonization, or cavitation of the corneocyte surface, except C. tropicalis, which showed intermediate results. Pepstatin, an inhibitor of Candida acid proteinase, did not alter adherence or cohesion formation, but inhibited formation of corneocyte cavitations about adherent blastoconidia, suggesting that this enzyme may facilitate adherence/invasion events on skin. Depletion of surface lipids did not alter the formation of cohesin material or the adherence process. Adherence and invasion of epithelium by pathogenic Candida species include the interaction of blastoconidia with an epithelial surface cohesin material that participates in the adherence process. Candida acid proteinase, a keratinolytic enzyme, may participate in the cavitation process of the corneocyte surface by C. albicans.
机译：念珠菌对表皮角质细胞的粘附是念珠菌定植和皮肤感染的早期事件。病原菌比非病原菌更能黏附，转化为菌丝生长，并侵入皮肤的角质层。使用六种念珠菌，通过扫描电子显微镜对实验性鼠科皮肤念珠菌感染进行粘附性研究。念珠菌念珠菌和念珠菌念珠菌（C. stellatoidea blastoconidia）应用于新生小鼠皮肤，其粘附于角质层的数量比其他测试物种要多，在孢子和角质细胞表面之间形成了原纤维和无定形粘液样物质（“粘着蛋白”）的链，形成了空化在角质细胞表面，并通过菌丝生长在远离母细胞介球菌附着点的位置侵入角质细胞包膜。除热带梭状芽胞杆菌外，其他物种对角质细胞表面的粘附，定植或空化几乎没有或没有，这显示了中间结果。 Pepstatin是念珠菌酸性蛋白酶的抑制剂，它不会改变粘附或内聚力的形成，但会抑制粘附的囊胚炎的角质细胞空洞的形成，表明该酶可能促进皮肤上的粘附/侵袭事件。表面脂质的消耗不会改变粘着素材料的形成或粘附过程。致病性念珠菌物种对上皮的粘附和侵袭包括胚芽孢杆菌与参与粘附过程的上皮表面粘附素物质的相互作用。白色念珠菌酸性蛋白酶（一种角蛋白分解酶）可能参与白色念珠菌对角质细胞表面的空化过程。

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