[P3-2-25] Expression and role of Dectin-1 in human oral epithelial cells
Keywords:Dectin-1、Candida albicans、antimicrobial peptides
Human oral epithelial cells serve as a crucial physical barrier to pathogens. They rapidly produce antimicrobial peptides and chemokines and induce local defense mechanisms after recognition of antigens through various receptors. Candida albicans is the predominant oral fungal pathogen. Its cell wall contains β-glucan which is recognized by Dectin-1, a C-type lectin. In this study, we investigated the expression and role of Dectin-1 in human oral epithelial cells. Flow cytometry revealed that human squamous epithelial cell lines: HSC-2, HSC-3, HSC-4 and Ca9-22 express Dectin-1. Real-time PCR showed that HSC-2 had the expression of Dectin-1, followed by Ca9-22. β-glucan induced the expression of antimicrobial peptides: β-defensin-1, S100A8, S100A9 and LL-37 in both HSC-2 and Ca9-22 cell lines. It also induced the expression of interleukin (IL)-6, IL-8 and IL-17F. Western blotting showed that β-glucan induced phosphorylation of spleen tyrosine kinase (Syk), a signaling molecule downstream of Dectin-1 as well as of p38, Akt and NF-κB. Their phosphorylation was suppressed after treatment with a Syk inhibitor. These results suggest that human oral epithelial cells recognize β-glucan derived from fungi through Dectin-1 and then activate Syk, which contributes to the maintenance of oral homeostasis.