E. coli LPS/TLR4/NF-κB Signaling Pathway Regulates Th17/Treg Balance Mediating Inflammatory Responses in Oral Lichen Planus

Oral lichen planus (OLP) is a chronic inflammatory autoimmune disease mediated by T cells. The imbalance of microflora has potential impacts on the onset and development of OLP, but the mechanism is still unclear. Here, we investigated the effects of Escherichia coli (E. coli) lipopolysaccharide (LPS) simulating the microbial enrichment state of OLP on T cell immune functions in vitro. Effect of E. coli LPS on the viability of T cell using CCK8 assay. After E. coli LPS pretreatment, the expression of the toll-like receptor 4 (TLR4), nuclear factor-kappa B p65 (NF-κB p65), cytokines, retinoic acid-related orphan receptor γt (RORγt), and forkhead box p3 (Foxp3) in the peripheral blood of OLP patients and normal controls (NC) were assessed using quantitative RT-PCR (qRT-PCR), western blot, and enzyme-linked immunosorbent assay (ELISA). Finally, Th17 and Treg cells were detected by flow cytometry. We found that the TLR4/NF-κB pathway was activated and the expression of interleukin (IL)-6 and IL-17 was increased in both groups after E. coli LPS stimulation. CC chemokine ligand (CCL)20 and CC chemokine receptor (CCR)4 expression was increased in OLP after E. coli LPS treatment, while no difference was found in CCR6 and CCL17 expression of both groups. Moreover, E. coli LPS treatment enhanced the proportion of Th17 cells, Th17/Treg ratio, and RORγt/Foxp3 ratio in OLP. In conclusion, E. coli LPS regulated Th17/Treg balance to mediate the inflammatory responses of OLP through the TLR4/NF-κB pathway in vitro, indicating that oral microbiota dysbiosis affected the chronic inflammatory state of OLP.