Lipoteichoic acid of Enterococcus faecalis interferes with Porphyromonas gingivalis lipopolysaccharide signaling via IRAK ‐M upregulation in human periodontal ligament cells

AbstractPeriodontitis is a chronic inflammatory disease of the gums caused by infection with multispecies oral bacteria. Since the periodontopathic bacteriaPorphyromonas gingivalis together withEnterococcus 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 andE. 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 MAP kinases, including 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 f or IL‐8 expression. Interestingly, Ef.LTA enhanced only IL‐1 receptor‐associated kinase‐M (IRAK‐M) expression among the tested negative regulators ...
Source: Molecular Oral Microbiology - Category: Microbiology Authors: Tags: ORIGINAL ARTICLE Source Type: research