<i><b>Porphyromonas gingivalis</b></i><b>-induced IL-33 down-regulates hCAP-18/LL-37 production in human gingival epithelial </b><b>cells </b>

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Author(s)

    • TADA Hiroyuki
    • Division of Oral Microbiology, Tohoku University Graduate School of Dentistry
    • SHIMIZU Takamitsu
    • Division of Oral Microbiology, 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>hCAP-18/LL-37 is an antimicrobial peptide that is mainly expressed in epithelial cells. Gingival epithelial cells play pivotal roles in antimicrobial defense by expressing hCAP-18/LL-37. <i>Porphyromonas gingivalis</i> is a primary pathogen for chronic periodontitis and produces cysteine proteinase gingipains, which induce proinflammatory cytokines production, leading to enhance inflammatory responses. In contrast, gingipains attenuate immune responses, leading to induce anti-inflammatory responses. In this study, we investigated the ability of gingipains to attenuate <i>P. gingivalis</i>-induced hCAP-18/LL-37 production by human gingival epithelial Ca9-22 cells. The expression of LL-37 mRNA was increased by the infection of Ca9-22 cells with a <i>P. gingivalis</i> gingipains-null mutant KDP136 compared with <i>P. gingivalis</i> wild-type strain ATCC 33277. Interleukin (IL)-33 is involved in the development of chronic inflammatory diseases, and <i>P. gingivalis</i> infection increases IL-33 production by human gingival epithelial cells. <i>P. gingivalis</i>-induced LL-37 mRNA expression was augmented in IL-33 small interfering RNA-transfected Ca9-22 cells. Maxacalcitol (22-oxacalcitriol: OCT) is a biologically active metabolite of vitamin D<sub>3</sub> analog, and OCT increases hCAP-18/LL-37 production by human gingival epithelial cells. The increasing expression of LL-37 mRNA by OCT was down-regulated by infection of the cells with <i>P. gingivalis</i> ATCC 33277 in Ca9-22 cells. Furthermore, <i>P. gingivalis</i> infection induced IL-33 mRNA expression in Ca9-22 cells; therefore, <i>P. gingivalis</i>-induced endogenous IL-33 down-regulated hCAP-18/LL-37 production by the bacterium. These findings suggested that endogenous IL-33 down-regulates the induction of hCAP-18/LL-37 production in human gingival epithelial cells.</p>

Journal

  • Biomedical Research

    Biomedical Research 38(3), 167-173, 2017

    Biomedical Research Press

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