Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells

Tada, Hiroyuki; Matsuyama, Takashi; Nishioka, Takashi; Hagiwara, Makoto; Kiyoura, Yusuke; Shimauchi, Hidetoshi; Matsushita, Kazunobu

doi:10.1371/journal.pone.0152794

Cited by 37 publications

(37 citation statements)

References 76 publications

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“…4A). Furthermore, IL-33 production in the culture supernatant from the cultures of the different stimulation times (12,24,72, and 96 h), which were stimulated with P. gingivalis whole cells, fimbriae, or PGTP2, also were quite low (2-5 pg/ mL), according to the ELISA findings (data not shown). Therefore, we examined intracellular IL-33 localization in BMDCs after stimulation with fimbriae or PGTP2 using immunocytochemical analysis.…”

Section: Discussion the Expression Of Il-33 Increases In Response Tomentioning

confidence: 94%

“…Accordthelium from patients with chronic periodontitis expresses IL-33, but scarcely in that from healthy individuals (11,24). We reported previously that the contaminant related to TLR2 activity in the P. gingivalis LPS fraction is lipoprotein (14).…”

Section: Discussion the Expression Of Il-33 Increases In Response Tomentioning

confidence: 96%

“…PAR-2-mediated IL-33 mRNA expression induced by gingipains from P. gingivalis is increased 48 h later in human gingival epithelial cells (24). Accordthelium from patients with chronic periodontitis expresses IL-33, but scarcely in that from healthy individuals (11,24).…”

Section: Discussion the Expression Of Il-33 Increases In Response Tomentioning

confidence: 99%

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

et al. 2017

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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. Porphyromonas gingivalis is a primary pathogen that is involved in chronic periodontitis and its bacterial components induce inflammatory responses. Dendritic cells (DCs) recognize pathogenassociated 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 P. gingivalis 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 P. gingivalis whole cells. Furthermore, fimbriae and lipopeptide derived from P. gingivalis exhibited higher IL-33 mRNA expression than P. gingivalis whole cells. In contrast, lipopolysaccharide derived from P. gingivalis 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

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Section: Discussion the Expression Of Il-33 Increases In Response Tomentioning

confidence: 94%

Section: Discussion the Expression Of Il-33 Increases In Response Tomentioning

confidence: 96%

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

et al. 2017

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“…These findings suggested that evasion of innate immune response by P. gingivalis is due to gingipains-mediated inhibition of antimicrobial peptide expression. Recently, we reported that P. gingivalis stimulation up-regulates intracellular IL-33 expression in human gingival/oral epithelial cells via gingipain-dependent mechanisms (30). To determine whether or not intracellular IL-33 participates in P. gingivalis-induced LL-37 induction, we reduced IL-33 mRNA expression in Ca9-22 cells using an IL-33-specific siRNA.…”

Section: Resultsmentioning

confidence: 99%

“…In contrast, IL-33 is also involved in the development of chronic inflammatory diseases (26). We reported recently that increasing expression of IL-33 is detected in gingival epithelium from patients with chronic periodontitis, and that gingipains from P. gingivalis increased intracellular IL-33 expression in human gingival epithelial cells (30). The function of intracellular IL-33 induced by P. gingivalis in gingival epithelial cells may involve the modulation of innate immune function and the pathogenesis of periodontal diseases.…”

Section: Reverse Transcription and Real-time Quantitative Polymerase mentioning

confidence: 98%

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

et al. 2017

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ABSTRACThCAP-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. Porphyromonas gingivalis 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 P. gingivalis-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 P. gingivalis gingipains-null mutant KDP136 compared with P. gingivalis wild-type strain ATCC 33277. Interleukin (IL)-33 is involved in the development of chronic inflammatory diseases, and P. gingivalis infection increases IL-33 production by human gingival epithelial cells. P. gingivalis-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 3 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 P. gingivalis ATCC 33277 in Ca9-22 cells. Furthermore, P. gingivalis infection induced IL-33 mRNA expression in Ca9-22 cells; therefore, P. gingivalis-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.

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Gingipains impair attachment of epithelial cell to dental titanium abutment surfaces

et al. 2019

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The study investigated in vitro the effect of Porphyromonas gingivalis and its cysteine proteases (gingipains) on epithelial cell adhesion to titanium–zirconium alloy surfaces. Titanium–zirconium discs with a standard machined (M) or chemically modified hydrophilic surface (modM) were coated with lamin‐5 and incubated with telomerase‐inactivated gingival keratinocytes (TIGK). Three P. gingivalis strains or gingipains were either added simultaneously with TIGK or after TIGK cells were already attached to the disks. Adhered TIGK cells were counted at 24 h. All P. gingivalis strains clearly inhibited adhesion of TIGK cells to M and modM surfaces. Compared with bacteria/gingipain‐free TIGK cell cultures, the number of attached TIGK cells was reduced by about 80% and 60% when P. gingivalis was added simultaneously or after TIGK cells were already attached to the disks (each p < 0.01), respectively. Counts of attached cells were similarly reduced when only gingipains were used. Adhesion molecules of TIGK cells, in particular E‐cadherin, were cleaved by P. gingivalis. In conclusion, P. gingivalis and gingipains interfere with the adhesion of epithelial cells to titanium–zirconium alloy surfaces by cleaving adhesion molecules, while a chemically modified hydrophilic titanium–zirconium alloy surface did not yield any protection. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B:2549–2556, 2019.

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Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells

Cited by 37 publications

References 76 publications

<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>

<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>

<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>

Gingipains impair attachment of epithelial cell to dental titanium abutment surfaces

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