Murine host response to Malassezia globosa colonization with and without skin barrier impairment based on whole transcriptome analysis.

Abstract

Malassezia is the most prevalent fungus on human skin and it acts as both a skin commensal and an opportunistic pathogen. It is involved in many inflammatory skin diseases. Here we report transcriptome analyses of skin tissues from murine models colonized by Malassezia globosa. The results showed that differentially expressed genes (DEGs) of both intact-skin group and barrier-impaired group were enriched in pathways including C-type lectin receptor signaling pathway, Toll-like receptor signaling pathway, NOD-like receptor signaling pathway, Fc epsilon RI signaling pathway, Fc gamma R-mediated phagocytosis, neutrophil extracellular trap formation, and IL-17 signaling pathway. Quantitative real-time PCR confirmed that genes encoding pattern recognition receptors (PRRs) such as Clec7a, Clec4n, Clec4e, Tlr1, Tlr2, Tlr4, Nlrp3, Nlrc4, and Nod2; genes related to neutrophil extracellular trap formation such as Padi4 and Camp; and genes involved in IL-17 signaling pathway such as Il17a, Il17f, and Il23a, were all upregulated both in intact murine skin and barrier-impaired murine skin. This study provides a transcriptional perspective on the mechanisms of host-Malassezia interactions. The genes related to the host responses caused by Malassezia are similar in intact and barrier-impaired skin, with host responses in barrier-impaired skin being more intense.