Adherence of Candida albicans and Malassezia Species to Skin Cells Induces Changes in the Expression of Genes Responsible for Heparan and Chondroitin Sulfate Chain Synthesis. / La unión de Candida albicans y Malassezia spp. a células de piel promueve cambios de expresión en los genes responsables de la síntesis de las cadenas de heparán y condroitín sulfato.

Superficial fungal infections are common in dermatology and are often caused by opportunistic species in the Candida and Malassezia genera. The aim of this study was to analyze changes in the expression of genes coding for enzymes involved in the biosynthesis of glycosaminoglycans (GAGs) chains following the adherence of Candida and Malassezia yeasts to skin cell lines. Gene expression was analyzed using reverse transcriptase-quantitative polymerase chain reaction assays. Interactions between the yeasts and the skin cells induced the following changes in genes involved in the biosynthesis of heparan sulfate and chondroitin sulfate: downregulation of CHPF in keratinocytes and downregulation of EXT1, EXT2, CHSY3, and CHPF in fibroblasts. Adherence to fibroblasts had an even greater effect on GAG biosynthetic enzymes, inducing the downregulation of 13 genes and the upregulation of two (CHST15 and CHST7). Interactions between yeasts and skin cells might affect the binding affinity of GAG chains, possibly changing their ability to function as receptors for pathogens and interfering with a key stage at the start of infection.

Glycosaminoglycans Are Involved in the Adhesion of Candida albicans and Malassezia Species to Keratinocytes But Not to Dermal Fibroblasts.

BACKGROUND AND 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. MATERIAL AND 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 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 Calbicans 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 Calbicans 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.

Glycosaminoglycans Are Involved in the Adhesion of Candida albicans and Malassezia Species to Keratinocytes But Not to Dermal Fibroblasts. / Los glicosaminoglicanos se encuentran implicados en la adherencia de Candida albicans y Malassezia spp. a queratinocitos, pero no a fibroblastos dérmicos.

BACKGROUND AND 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. MATERIAL AND 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.