Literature DB >> 20412419

Interleukin-1 receptor-associated kinase-M in gingival epithelial cells attenuates the inflammatory response elicited by Porphyromonas gingivalis.

N Takahashi1, T Honda, H Domon, T Nakajima, K Tabeta, K Yamazaki.   

Abstract

BACKGROUND AND
OBJECTIVE: Recent studies have revealed that negative regulatory molecules, including interleukin-1 receptor-associated kinase-M (IRAK-M), control the overactivation of Toll-like receptor (TLR) signaling. The role of IRAK-M in human gingival epithelial cells (HGECs), which express TLRs, remains unclear. The present study examined the role of IRAK-M on interleukin-8 and macrophage chemoattractant protein-1 (MCP-1) expression in HGECs stimulated with Porphyromonas gingivalis and TLR ligands.
MATERIAL AND METHODS: Primary HGECs and an SV40 T-antigen-immortalized HGEC line (epi 4) were stimulated with live or heat-killed P. gingivalis, P. gingivalis lipopolysaccharide or the synthetic lipopeptide PAM(3)CSK(4), and subsequent expression of IRAK-M, interleukin-8 and MCP-1 was evaluated at the mRNA and protein levels. The effects of IRAK-M on interleukin-8 and MCP-1 expressions were evaluated by IRAK-M-specific RNA interference (RNAi)-based loss-of-function assay.
RESULTS: All tested stimulants up-regulated the expression of IRAK-M in HGECs. The P. gingivalis lipopolysaccharide or PAM(3)CSK(4) increased MCP-1 expression, whereas live P. gingivalis down-regulated the MCP-1 expression in HGECs. However, IRAK-M RNAi increased the expression of MCP-1 irrespective of up- or down-regulation mediated by the respective stimulants. Interleukin-8 gene expression, up-regulated by all tested stimulants, was further enhanced by IRAK-M RNAi. In contrast, IRAK-M RNAi had no effect on the interleukin-8 protein levels, irrespective of the stimulant, indicating that post-translational modification, not IRAK-M, controls interleukin-8 protein expression.
CONCLUSION: Interleukin-1 receptor-associated kinase-M appeared to have distinct regulatory roles on the interleukin-8 and MCP-1 produced by HGECs, further suggesting an important role for interleukin-8 in the immune response to periodontopathic bacteria.

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Year:  2010        PMID: 20412419     DOI: 10.1111/j.1600-0765.2009.01266.x

Source DB:  PubMed          Journal:  J Periodontal Res        ISSN: 0022-3484            Impact factor:   4.419


  10 in total

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2.  Epithelial TRPV1 signaling accelerates gingival epithelial cell proliferation.

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5.  Macrophage HIF-1α mediates obesity-related adipose tissue dysfunction via interleukin-1 receptor-associated kinase M.

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Authors:  Chuan Wang; Tianfan Cheng; Xuan Li; Lijian Jin
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Review 8.  Lactobacillus-Derived Bioactive Metabolites for the Regulation of Periodontal Health: Evidences to Clinical Setting.

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Journal:  Molecules       Date:  2020-04-29       Impact factor: 4.411

9.  IRAK-M expression limits dendritic cell activation and proinflammatory cytokine production in response to Helicobacter pylori.

Authors:  Jessica Shiu; Steven J Czinn; Koichi S Kobayashi; Yezhou Sun; Thomas G Blanchard
Journal:  PLoS One       Date:  2013-06-11       Impact factor: 3.240

10.  A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling.

Authors:  Miki Yamada; Naoki Takahashi; Yumi Matsuda; Keisuke Sato; Mai Yokoji; Benso Sulijaya; Tomoki Maekawa; Tatsuo Ushiki; Yoshikazu Mikami; Manabu Hayatsu; Yusuke Mizutani; Shigenobu Kishino; Jun Ogawa; Makoto Arita; Koichi Tabeta; Takeyasu Maeda; Kazuhisa Yamazaki
Journal:  Sci Rep       Date:  2018-06-13       Impact factor: 4.379

  10 in total

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