Dectin-1/SYK Activation Induces Antimicrobial Peptide and Negative Regulator of NF-ĸB Signaling in Human Oral Epithelial Cells

Background/Aim: Oral epithelial cells serve as the primary defense against microbial exposure in the oral cavity, including the fungus Candida albicans. Dectin-1 is crucial for recognition of /i-glucan in fungi. However, expression and function of Dectin-1 in oral epithelial cells remain unclear. Materials and Methods: We assessed Dectin1 expression in Ca9-22 (gingiva), HSC-2 (mouth), HSC-3 (tongue), and HSC-4 (tongue) human oral epithelial cells using flow cytometry and real-time polymerase chain reaction. Cell treated with /i-glucan-rich zymosan were evaluated using real-time polymerase chain reaction. Phosphorylation of spleen-associated tyrosine kinase (SYK) was analyzed by western blotting. Results: Dectin-1 was expressed in all four cell types, with high expression in Ca922 and HSC-2. In Ca9-22 cells, exposure to /i-glucan-rich zymosan did not alter the mRNA expression of chemokines nor of interleukin (IL)6, IL8, IL1/i, IL17A, and IL17F. Zymosan induced the expression of antimicrobial peptides /idefensin-1 and LL-37, but not S100 calcium-binding protein A8 (S100A8) and S100A9. Furthermore, the expression of cylindromatosis (CYLD), a negative regulator of nuclear factor kappa B (NF-& kgreen;B) signaling, was induced. In HSC-2 cells, zymosan induced the expression of IL17A. The expression of tumor necrosis factor alpha -induced protein 3 (TNFAIP3), a negative regulator of NF-& kgreen;B signaling, was also induced. Expression of other cytokines and antimicrobial peptides remained unchanged. Zymosan induced phosphorylation of SYK in Ca9-22 cells, as well as NF-& kgreen;B. Conclusion: Oral epithelial cells express Dectin-1 and recognize /i-glucan, which activates SYK and induces the expression of antimicrobial peptides and negative regulators of NF-& kgreen;B, potentially maintaining oral homeostasis.