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Porphyromonas gingivalis lipopolysaccharide induces over production of CC chemokine ligand 2 via toll‐like receptor‐4 in oral lichen planus
Author(s) -
Zeng Qi,
Yang Xi,
Chen Xiaobing,
Xia Juan,
Cheng Bin,
Tao Xiaoan
Publication year - 2018
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12655
Subject(s) - porphyromonas gingivalis , oral lichen planus , lipopolysaccharide , chemokine , pathogenesis , chemistry , toll like receptor , receptor , downregulation and upregulation , epithelium , microbiology and biotechnology , immunology , biology , innate immune system , pathology , medicine , periodontitis , biochemistry , gene
Background We recently reported that the CC chemokine ligand 2 ( CCL 2)‐ CC receptor 2 ( CCR 2) axis was involved in the pathogenesis of oral lichen planus ( OLP ). However, the exact mechanism for the high expression of CCL 2 in OLP specimens is not clear. Therefore, this study was designed to investigate the potential role of the toll‐like receptor 4 ( TLR ‐4) pathway in overproduction of CCL 2 in OLP lesions. Methods Immunohistochemical staining and real‐time RT ‐ PCR were used to detect TLR ‐4, CCL 2, and CCR 2 expression in OLP lesions. Then, gingival epithelial cells from OLP lesions were established and treated with Porphyromonas gingivalis ( P. gingivalis) lipopolysaccharide ( LPS ). CCL 2 expression in epithelial cells was determined by Western blotting and real‐time RT ‐ PCR . In some experiments, TAK ‐242, a specific inhibitor of TLR ‐4, was used to block the TLR ‐4 pathway before cells were stimulated with LPS . Results We found that TLR ‐4 was significantly increased in the epithelium of OLP specimens, compared with controls. Moreover, LPS can induce the over production of CCL 2 in epithelial cells of OLP , in vitro. TAK ‐242 effectively eliminated the increase in CCL 2 expression induced by LPS by blocking the TLR ‐4/ NF ‐κB pathway. In addition, we again confirmed that expression of CCL 2 and CCR 2 was increased in OLP specimens. Conclusion Increased TLR ‐4 expression contributes to the upregulated expression of CCL 2 in the epithelium of OLP lesions, which suggests that oral bacteria participate in the pathogenesis of OLP via the TLR ‐4 pathway.