Mast Cells Contribute to<i>Porphyromonas gingivalis–</i>induced Bone Loss

Malcolm, Jennifer; Millington, Owain R.; Millhouse, Emma; Campbell, Louisa; Planell, A. Adrados; Butcher, John; Lawrence, Catherine E.; Ross, Kirsty; Ramage, Gordon; McInnes, Iain B.; Culshaw, Shauna

doi:10.1177/0022034516634630

Cited by 26 publications

(25 citation statements)

References 43 publications

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“…IL‐31 activates epidermal keratinocytes, intestinal epithelial cells, or subepithelial myofibroblasts to secrete inflammatory cytokines and chemokines (Dambacher et al, ; Dillon et al, ; Ip et al, ; Yagi et al, ). Increased expression of TNF‐α, IL‐6, and IL‐1β mRNA was recently observed in the gingiva of WT mice, but not in mast cell‐deficient mice, following oral P. gingivalis infection (Malcolm et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Mast cells accumulate at inflammatory site of periodontal tissue of patients with chronic periodontitis (E Ribeiro, dos Santos, Rocha, & Cury, ; Huang et al, ) and produce TGF‐β, matrix metalloproteinases, tissue inhibitors of metalloproteinases, or IL‐17, leading to the destruction of periodontal tissues (Myint et al, ; Naesse et al, ; Parachuru, Coates, Milne, Rich, & Seymour, ). Moreover, mast cells release TNF‐α and IL‐6 in response to P. gingivalis infection and induce alveolar bone loss in mice (Malcolm et al, ). These findings imply that the mast cell‐derived mediators may play a role in exacerbation of inflammation in the periodontal tissues.…”

Section: Discussionmentioning

confidence: 99%

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Porphyromonas gingivalisinduces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier

Tada

Nishioka

Takase

et al. 2018

Cellular Microbiology

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Interleukin (IL)‐31 is important for innate immunity in mucosal tissues and skin, and increased IL‐31 expression participates in the pathogenesis of chronic inflammatory diseases affecting the skin, airways, lungs, and intestines. We investigated the contribution of mast cells to the induction of IL‐31 production following infection with the periodontal pathogen, Porphyromonas gingivalis. We found that oral infection with P. gingivalis increased IL‐31 expression in the gingival tissues of wild‐type mice but not in those of mast cell‐deficient mice. The P. gingivalis‐induced IL‐31 production by human mast cells occurred through the activation of the JNK and NF‐κB signalling pathways and was dependent on the P. gingivalis lysine‐specific protease gingipain‐K. P. gingivalis infection induced IL‐31 receptor α and oncostatin M receptor β expression in human gingival epithelial cells. Notably, the P. gingivalis‐induced IL‐31 production by mast cells led to the downregulation of claudin‐1, a tight junction molecule, in gingival epithelial cells, resulting in an IL‐31‐dependent increase in the paracellular permeability of the gingival epithelial barrier. These findings suggest that IL‐31 produced by mast cells in response to P. gingivalis infection causes gingival epithelial barrier dysfunction, which may contribute to the chronic inflammation observed in periodontitis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalisinduces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier

Tada

Nishioka

Takase

et al. 2018

Cellular Microbiology

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“…Ten-species biofilms were built up on Thermanox coverslips as detailed elsewhere [16, 19] in the following order: an initial 3-species biofilm consisting of S . mitis , S .…”

Section: Methodsmentioning

confidence: 99%

In Vitro Effect of Porphyromonas gingivalis Methionine Gamma Lyase on Biofilm Composition and Oral Inflammatory Response

et al. 2016

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Methanethiol (methyl mercaptan) is an important contributor to oral malodour and periodontal tissue destruction. Porphyromonas gingivalis, Prevotella intermedia and Fusobacterium nucleatum are key oral microbial species that produce methanethiol via methionine gamma lyase (mgl) activity. The aim of this study was to compare an mgl knockout strain of P. gingivalis with its wild type using a 10-species biofilm co-culture model with oral keratinocytes and its effect on biofilm composition and inflammatory cytokine production. A P. gingivalis mgl knockout strain was constructed using insertion mutagenesis from wild type W50 with gas chromatographic head space analysis confirming lack of methanethiol production. 10-species biofilms consisting of Streptococcus mitis, Streptococcus oralis, Streptococcus intermedius, Fusobacterium nucleatum ssp polymorphum, Fusobacterium nucleatum ssp vincentii, Veillonella dispar, Actinomyces naeslundii, Prevotella intermedia and Aggregatibacter actinomycetemcomitans with either the wild type or mutant P. gingivalis were grown on Thermanox cover slips and used to stimulate oral keratinocytes (OKF6-TERT2), under anaerobic conditions for 4 and 24 hours. Biofilms were analysed by quantitative PCR with SYBR Green for changes in microbial ecology. Keratinocyte culture supernatants were analysed using a multiplex bead immunoassay for cytokines. Significant population differences were observed between mutant and wild type biofilms; V. dispar proportions increased (p<0.001), whilst A. naeslundii (p<0.01) and Streptococcus spp. (p<0.05) decreased in mutant biofilms. Keratinocytes produced less IL-8, IL-6 and IL-1α when stimulated with the mutant biofilms compared to wild type. Lack of mgl in P. gingivalis has been shown to affect microbial ecology in vitro, giving rise to a markedly different biofilm composition, with a more pro-inflammatory cytokine response from the keratinocytes observed. A possible role for methanethiol in biofilm formation and cytokine response with subsequent effects on oral malodor and periodontitis is suggested.

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“…IL‐6 could induce osteoclastogenesis and accelerate pathogenesis of periodontal disease 47 . TNF‐α and IL‐1 play critical roles in the immunopathogenesis of periodontitis, and IL‐1 has been thought to be a potential candidate for genetic biomarkers of periodontitis 48,49 . Elevated IL‐8, IL‐1β, and TNF‐α levels were observed in inflamed periodontal tissue 50 .…”

Section: Discussionmentioning

confidence: 99%

Metformin Inhibits Porphyromonasgingivalis Lipopolysaccharide‐Influenced Inflammatory Response in Human Gingival Fibroblasts via Regulating Activating Transcription Factor‐3 Expression

Kang

Wang

et al. 2017

Journal of Periodontology

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Mast Cells Contribute toPorphyromonas gingivalis–induced Bone Loss

Abstract: word count: 246 11Total word count (Abstract to Acknowledgments): 3493 12

Cited by 26 publications

References 43 publications

Porphyromonas gingivalisinduces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier

Porphyromonas gingivalisinduces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier

In Vitro Effect of Porphyromonas gingivalis Methionine Gamma Lyase on Biofilm Composition and Oral Inflammatory Response

Metformin Inhibits Porphyromonasgingivalis Lipopolysaccharide‐Influenced Inflammatory Response in Human Gingival Fibroblasts via Regulating Activating Transcription Factor‐3 Expression

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