<b>Increases in IL-33 production by fimbriae and lipopeptide from </b><i><b>Porphyromonas gingivalis</b></i><b> in mouse bone marrow-derived dendritic cells via Toll-like receptor </b><b>2 </b>

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Author(s)

    • TADA Hiroyuki
    • Division of Oral Microbiology, Tohoku University Graduate School of Dentistry
    • SUZUKI Risako
    • Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
    • NEMOTO Eiji
    • Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
    • SHIMAUCHI Hidetoshi
    • Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
    • MATSUSHITA Kenji
    • Department of Oral Disease Research, National Center for Geriatrics and Gerontology
    • TAKADA Haruhiko
    • Division of Oral Microbiology, Tohoku University Graduate School of Dentistry

Abstract

<p>Interleukin-33 (IL-33) is an IL-1 cytokine family member that is involved in the development of chronic inflammatory diseases and the initiation of allergic inflammation in response to pathogens. <i>Porphyromonas gingivalis</i> is a primary pathogen that is involved in chronic periodontitis and its bacterial components induce inflammatory responses. Dendritic cells (DCs) recognize pathogen- associated molecular patterns by expression of pattern-recognition receptors, such as Toll-like receptors (TLRs). DCs play an essential role in resistance to infection and maintenance of mucosal immune system. In this study, we investigated whether <i>P. gingivalis</i> increases the expression of IL-33 in mouse bone marrow-derived DCs (BMDCs). BMDCs exhibited an increased expression of IL-33 mRNA upon stimulation with <i>P. gingivalis</i> whole cells. Furthermore, fimbriae and lipopeptide derived from <i>P. gingivalis</i> exhibited higher IL-33 mRNA expression than <i>P. gingivalis</i> whole cells. In contrast, lipopolysaccharide derived from <i>P. gingivalis</i> did not induce IL-33 mRNA expression in BMDCs. The IL-33 mRNA expression after stimulation with fimbriae or lipopeptide was up-regulated in BMDCs from wild-type mice but not from TLR2-deficient (TLR2<sup>−/−</sup>) mice. IL-33 production induced by fimbriae and lipopeptide accumulated in the cytoplasm of BMDCs from wild-type mice, but not from TLR2<sup>−/−</sup> mice. These findings suggested that IL-33 production induced by <i>P. gingivalis</i> fimbriae and lipopeptide is recognized by TLR2 and may modulate DC function in periodontal diseases.</p>

Journal

  • Biomedical Research

    Biomedical Research 38(3), 189-195, 2017

    Biomedical Research Press

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