Recombinant human interleukin 17A enhances the anti-Candida effect of human oral mucosal epithelial cells by inhibiting Candida albicans growth and inducing antimicrobial peptides secretion.

Abstract

Candida albicans (Calbicans) is the most common fungal pathogen causing opportunistic infections. IL17 (IL17A) is a vital mediator of antifungal immunity. The aim of the study was to investigate the effect of recombinant human interleukin 17A (rhIL17A) on human oral mucosal epithelial cells (hOMECs) defending against Calbicans infection. Human oral mucosal epithelial cells were divided into four groups: Calbicans+ (MOI=0.1), rhIL17A+ (100μg/L), rhIL17A+Calbicans+ (MOI=0.1, rhIL17A:100μg/L) and blank control. Then, Calbicans growth was observed after 24hours. Human beta-2 defensin (hBD-2), S100A8 and LL-37 in supernatants and their mRNAs in cells were measured by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction, respectively. In Calbicans+ group, Calbicans hyphae formation and the death of infected hOMECs were observed. However, in the rhIL17A+Calbicans+ group, IL17 inhibited both hypha formation, and Calbicans from infecting hOMECs and its further growth. There was no statistical significance in adhesion rates of Calbicans to hOMECs. Compared with the control group, the level of hBD-2 mRNA has increased, while hBD-2 and hBD-2 mRNA levels in the rhIL17A+Calbicans+ group were the highest. Both hBD-2 and hBD-2 mRNA levels were higher in the rhIL17A+ group than in the Calbicans+ group. S100A8 and LL-37 mRNAs have similar trend, and both upregulated after treatment with rhIL17A; however, protein levels were undetectable. Recombinant human interleukin 17A may inhibit Calbicans from infecting hOMECs by affecting the growth and reproduction of Calbicans as well as the formation of hyphae. Besides, rhIL17A might induce hBD-2, S100A8 and LL-37 secretion from hOMECs to strengthen their anti-infective ability.