Abstract
Ulcerative Colitis (UC) has been reported to be related to Porphyromonas gingivalis (P. gingivalis). Porphyromonas gingivalis peptidylarginine deiminase (PPAD), a virulence factor released by P. gingivalis, is known to induce inflammatory responses. To explore the pathological relationships between PPAD and UC, we used homologous recombination technology to construct a P. gingivalis strain in which the PPAD gene was deleted (Δppad) and a Δppad strain in which the PPAD gene was restored (comΔppad). C57BL/6 mice were orally gavaged with saline, P. gingivalis, Δppad, or comΔppad twice a week for the entire 40 days (days 0−40), and then, UC was induced by dextran sodium sulfate (DSS) solution for 10 days (days 31−40). P. gingivalis and comΔppad exacerbated DDS-induced colitis, which was determined by assessing the parameters of colon length, disease activity index, and histological activity index, but Δppad failed to exacerbate DDS-induced colitis. Flow cytometry and ELISA revealed that compared with Δppad, P. gingivalis, and comΔppad increased T helper 17 (Th17) cell numbers and interleukin (IL)-17 production but decreased regulatory T cells (Tregs) numbers and IL-10 production in the spleens of mice with UC. We also cocultured P. gingivalis, Δppad, or comΔppad with T lymphocytes in vitro and found that P. gingivalis and comΔppad significantly increased Th17 cell numbers and decreased Treg cell numbers. Immunofluorescence staining of colon tissue paraffin sections also confirmed these results. The results suggested that P. gingivalis exacerbated the severity of UC in part via PPAD.
Highlights
Periodontitis, the most common oral infectious disease caused by bacterial biofilms, results in the loss of periodontal attachment and alveolar bone, and it is a major etiology of tooth loss in adults[1]
We explored the significant effect of P. gingivalis on ulcerative colitis (UC), which resulted in the exacerbation of inflammation in a mouse model
P. gingivalis exacerbated the intestinal inflammation of mice treated with dextran sodium sulfate (DSS) After 19 days of pretreatment, mice were inoculated with P. gingivalis strains on day 0 (Fig. 1a)
Summary
Periodontitis, the most common oral infectious disease caused by bacterial biofilms, results in the loss of periodontal attachment and alveolar bone, and it is a major etiology of tooth loss in adults[1]. The activation of intestinal mucosal immune responses is the immediate cause of the occurrence and development of UC and affects its prognosis[4]. Oral bacteria derived from periodontitis may translocate to the intestine, and together with the intestinal microbiome, cause intestinal epithelial cell barrier dysfunction and amplify intestinal inflammation[7]. Oral infection with Porphyromonas gingivalis impairs colonic motor functions, suggesting that periodontal pathogens can be defined as regulators of the host response in IBD11,12. Proinflammatory cytokines produced and activated locally in the oral cavity might enter the bloodstream and circulate to the intestines, impacting IBD13,14. This evidence indicates that periodontitis may be closely related to colitis through a substantially altered microbiome
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