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Abstract：
OBJECTIVE: Superficial mycoses are some of the most common diseases worldwide. The usual culprits - yeasts belonging to the genera Malassezia and Candida - are commensal species in the skin that can cause opportunistic infections. We aimed to determine whether these yeasts use glycosaminoglycans (GAGs) as adhesion receptors to mediate binding to epithelial cells.
METHODS: In keratinocyte and dermal fibroblast cultures, we used rhodamine B and genistein to inhibit GAG synthesis to study the role these molecules play in the adhesion of Candida albicans (C. albicans) and Malassezia species to cells. We also analyzed GAG involvement by means of enzyme digestion, using specific lyases.
RESULTS: Rhodamine B partially inhibited the adhesion of both fungi to keratinocytes but not to fibroblasts. Selective digestion of heparan sulfate enhanced the binding of Malassezia species to keratinocytes and of both fungi to fibroblasts. Chondroitin sulfate digestion decreased C. albicans adhesion to keratinocytes, but increased the adhesion of the filamentous forms of this species to fibroblasts.
CONCLUSIONS: Cell surface GAGs appear to play a role in the adhesion of C albicans and Malasezzia species to keratinocytes. In contrast, their adhesion to fibroblasts appears to be enhanced by GAG inhibition, suggesting that some other type of receptor is the mediator.
METHODS: In keratinocyte and dermal fibroblast cultures, we used rhodamine B and genistein to inhibit GAG synthesis to study the role these molecules play in the adhesion of Candida albicans (C. albicans) and Malassezia species to cells. We also analyzed GAG involvement by means of enzyme digestion, using specific lyases.
RESULTS: Rhodamine B partially inhibited the adhesion of both fungi to keratinocytes but not to fibroblasts. Selective digestion of heparan sulfate enhanced the binding of Malassezia species to keratinocytes and of both fungi to fibroblasts. Chondroitin sulfate digestion decreased C. albicans adhesion to keratinocytes, but increased the adhesion of the filamentous forms of this species to fibroblasts.
CONCLUSIONS: Cell surface GAGs appear to play a role in the adhesion of C albicans and Malasezzia species to keratinocytes. In contrast, their adhesion to fibroblasts appears to be enhanced by GAG inhibition, suggesting that some other type of receptor is the mediator.
摘要：
目的：浅表真菌病是世界范围内最常见的一些疾病。通常的罪魁祸首-属于马拉色菌属和念珠菌属的酵母-是皮肤中的共生物种，可引起机会性感染。我们旨在确定这些酵母是否使用糖胺聚糖（GAG）作为粘附受体来介导与上皮细胞的结合。
方法：在角质形成细胞和真皮成纤维细胞培养物中，我们使用罗丹明B和金雀异黄素抑制GAG合成，以研究这些分子在白色念珠菌粘附中的作用(C.白色念珠菌）和马拉色菌物种到细胞。我们还通过酶消化分析了GAG的参与，使用特定的裂解酶。
结果：罗丹明B部分抑制两种真菌对角质形成细胞的粘附，但不抑制成纤维细胞的粘附。硫酸乙酰肝素的选择性消化增强了马拉色菌物种与角质形成细胞的结合以及两种真菌与成纤维细胞的结合。硫酸软骨素消化减少白色念珠菌对角质形成细胞的粘附，但是增加了该物种的丝状形式与成纤维细胞的粘附。
结论：细胞表面GAG似乎在白色念珠菌和Malasezzia物种与角质形成细胞的粘附中起作用。相比之下,它们与成纤维细胞的粘附似乎被GAG抑制增强，表明其他类型的受体是介体。
方法：在角质形成细胞和真皮成纤维细胞培养物中，我们使用罗丹明B和金雀异黄素抑制GAG合成，以研究这些分子在白色念珠菌粘附中的作用(C.白色念珠菌）和马拉色菌物种到细胞。我们还通过酶消化分析了GAG的参与，使用特定的裂解酶。
结果：罗丹明B部分抑制两种真菌对角质形成细胞的粘附，但不抑制成纤维细胞的粘附。硫酸乙酰肝素的选择性消化增强了马拉色菌物种与角质形成细胞的结合以及两种真菌与成纤维细胞的结合。硫酸软骨素消化减少白色念珠菌对角质形成细胞的粘附，但是增加了该物种的丝状形式与成纤维细胞的粘附。
结论：细胞表面GAG似乎在白色念珠菌和Malasezzia物种与角质形成细胞的粘附中起作用。相比之下,它们与成纤维细胞的粘附似乎被GAG抑制增强，表明其他类型的受体是介体。
