IFN-β secretion is through TLR3 but not TLR4 in human gingival epithelial cells.

The oral cavity is home for a plethora of bacteria and viruses. Epithelial barriers encounter these micro-organisms and recognize them via pathogen recognition receptors (PRRs) that instigate antibacterial and antiviral responses. We and others have shown that human gingival epithelial cells (HGECs) express PRRs to defend invading pathogens. Among these PRRs, TLR2, TLR3 and TLR4 are highly expressed in HGECs and appear to be important based on our previous findings. IFN-β is one of the major type 1 interferons induced to defend viral attack. In this report, we sought to dissect TLR3 and TLR4 mediated secretion of IFN-β in HGECs. We stimulated HGECs with ultrapure LPS (TLR4 ligand) and Poly I:C (TLR3 ligand) for 24 h and supernatant was used to determine IFN-β secretion. We show that cells treated with Poly I:C induced IFN-β secretion but not cells treated with LPS. In addition, silencing of TLR3 prior to Poly I:C stimulation significantly downregulated IFN-β secretion. On the contrary, overexpression of MD2 and TLR4 in HGECs restored IFN-β secretion. Upon further evaluation, we found that TLR3 stimulation but not TLR4 induced the phosphorylation of interferon regulatory factor 3 (IRF3), which is critical for IFN-β secretion. We conclude that IFN-β secretion is through TLR3 and not via TLR4 in HGECs.

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