Ray T L, Payne C D
Marshall Dermatology Research Laboratories, Department of Dermatology, University of Iowa College of Medicine, Iowa City 52242.
Infect Immun. 1988 Aug;56(8):1942-9. doi: 10.1128/iai.56.8.1942-1949.1988.
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.
芽生孢子黏附于表皮角质形成细胞是念珠菌在皮肤定植和感染的早期事件。致病性念珠菌比非致病性念珠菌更易黏附，转变为菌丝生长，并侵入皮肤角质层。通过扫描电子显微镜对实验性小鼠皮肤念珠菌感染进行研究，使用了六种念珠菌。将白色念珠菌和星状念珠菌的芽生孢子应用于新生小鼠皮肤，它们黏附于角质层的数量比其他受试菌种更多，在孢子与角质形成细胞表面之间获得了无定形黏蛋白样物质（“黏附素”）的纤维和条索，在角质形成细胞表面形成空泡，并通过在远离芽生孢子附着点的部位以菌丝生长的方式侵入角质形成细胞包膜。其他菌种除热带念珠菌显示出中等结果外，几乎没有或没有角质形成细胞表面的黏附、定植或空泡形成。胃蛋白酶抑制剂，一种念珠菌酸性蛋白酶的抑制剂，并没有改变黏附或黏附素的形成，但抑制了围绕黏附芽生孢子的角质形成细胞空泡的形成，这表明这种酶可能促进皮肤表面的黏附/侵入事件。表面脂质的耗尽并没有改变黏附素物质的形成或黏附过程。致病性念珠菌种对上皮的黏附和侵入包括芽生孢子与参与黏附过程的上皮表面黏附素物质的相互作用。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形成细胞表面的空泡化过程。
