Abstract

Oral lichen planus (OLP) is a T-cell-mediated immunoinflammatory disease. Several studies have proposed that Escherichia coli ( E. coli ) may participate in the progress of OLP. In this study, we examined the functional role of E. coli and its supernatant via toll-like receptor 4 (TLR4)/nuclear factor-kappab (NF-κB) signaling pathway in regulating T helper (Th) 17/ regulatory T (Treg) balance and related cytokines and chemokines profile in OLP immune microenvironment. We discovered that E. coli and supernatant could activate the TLR4/NF-κB signaling pathway in human oral keratinocytes (HOKs) and OLP-derived T cells and increase the expression of interleukin (IL)-6, IL-17, C‐C motif chemokine ligand (CCL) 17 and CCL20, thereby increasing the expression of retinoic acid-related orphan receptor (RoRγt) and the proportion of Th17 cells. Furthermore, the co-culture experiment revealed that HOKs treated with E. coli and supernatant increased T cell proliferation and migration, which promoted HOKs apoptosis. TLR4 inhibitor (TAK-242) successfully reversed the effect of E. coli and its supernatant. Consequently, E. coli and supernatant activated the TLR4/NF-κB signaling pathway in HOKs and OLP-derived T cells, leading to increased cytokines and chemokines expression and Th17/Treg imbalance in OLP.