Our skin provides immunological protection against several pathogens. Skin epithelial cells respond to microbial stimuli in various ways, such as through the production of antimicrobial peptides or secretion of cytokines, although phagocytosis of potentially evading microbes was also reported.

Relatively little is known about how skin keratinocytes differentiate between the presence of pathogenic and commensal fungi. In this project, we aimed to investigate how human keratinocytes interact with different species, as common colonizers of the skin. While is a common cause of cutaneous candidiasis, rarely associated with this disease.For the experimentshuman skin keratinocyte cell lines (HaCaT, HPV-KER)were applied andchallengedwith (SC5314 and WO1 strains) and (GA1 and CLIB214 strains)strains.We aimedto determine the extent to which and damage human keratinocytes, their attachment to host cells, the keratinocytes’ ability to internalize these fungi and to examinecytokine production in response to stimuli.

Our results suggest that causes significantly more damage to human keratinocytes than and the HPV-KER cell line was more susceptibleto the infection. In both HaCaT and HPV-KER cells, the production of IL-6, IL-8, and CCL5 increased primarilyafter infection. Based on the adhesion studies, there was a low degree of association in case of GA1 and CLIB214 compared to SC5314 and WO1.

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