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  • Title: Lipoteichoic acid of Enterococcus faecalis interferes with Porphyromonas gingivalis lipopolysaccharide signaling via IRAK-M upregulation in human periodontal ligament cells.
    Author: Im J, Baik JE, Lee D, Kum KY, Yun CH, Park OJ, Han SH.
    Journal: Mol Oral Microbiol; 2020 Aug; 35(4):146-157. PubMed ID: 32311229.
    Abstract:
    Periodontitis is a chronic inflammatory disease of the gum caused by infection with multispecies oral bacteria. Since the periodontopathic bacteria, Porphyromonas gingivalis together with Enterococcus faecalis are frequently detected in patients with a severe form of periodontitis, interactions between their virulence factors might play an important role in progression of the disease. P. gingivalis and E. faecalis possess lipopolysaccharide (Pg.LPS) and lipoteichoic acid (Ef.LTA), respectively, as the major virulence factors inducing inflammatory responses. However, the combinatorial effect of these virulence factors on chemokine expression was poorly understood. Here, we examined the interaction between Ef.LTA and Pg.LPS on IL-8 induction in human periodontal ligament (PDL) cells. Pg.LPS, but not Ef.LTA, induced IL-8 expression at both mRNA and protein levels, which was suppressed in the presence of Ef.LTA. Although Ef.LTA and Pg.LPS could stimulate Toll-like receptor 2 (TLR2), Ef.LTA did not interfere with Pg.LPS induced-TLR2 activation. However, Ef.LTA decreased Pg.LPS-induced phosphorylation of ERK, JNK, and p38 kinase. Furthermore, Ef.LTA suppressed Pg.LPS-induced IL-8 promoter activity as well as AP-1, NF-IL6 and NF-κB transcription factors, which are indispensable for IL-8 expression. Interestingly, Ef.LTA enhanced only IL-1 receptor-associated kinase-M (IRAK-M) expression among the tested negative regulators of TLR intracellular signaling cascades in the presence of Pg.LPS. In addition, silencing IRAK-M restored the decreased IL-8 expression by Ef.LTA in the presence of Pg.LPS. Collectively, these results suggest that Ef.LTA inhibits Pg.LPS-induced IL-8 expression in human PDL cells via inducing the expression of a negative regulator of TLR signaling cascades, IRAK-M.
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