4.7 Article

Periodontitis Salivary Microbiota Worsens Colitis

期刊

JOURNAL OF DENTAL RESEARCH
卷 101, 期 5, 页码 559-568

出版社

SAGE PUBLICATIONS INC
DOI: 10.1177/00220345211049781

关键词

periodontal diseases; colonic diseases; saliva; gut microbiota; swallowing; systemic health; disease

资金

  1. National Natural Science Foundation of China [81970939]
  2. Nanjing Clinical Research Center for Oral Diseases [2019060009]
  3. Project of Invigorating Health Care Through Science, Technology and Education [CXTDB2017014]

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The study investigated the impact and mechanisms of periodontitis salivary microbiota on colonic inflammation. Results showed that in the periodontitis colitis model, salivary microbiota exacerbated colitis, resembling the pathology of ulcerative colitis.
Evidence suggests that periodontitis contributes to the pathogenesis of inflammatory bowel disease, including Crohn's disease and ulcerative colitis. However, few studies have examined the role of swallowing and saliva in the pathogenesis of gastrointestinal diseases. Saliva contains an enormous number of oral bacteria and is swallowed directly into the intestine. Here, we explored the influence of periodontitis salivary microbiota on colonic inflammation and possible mechanisms in dextran sulfate sodium (DSS)-induced colitis. The salivary microbiota was collected from healthy individuals and those with periodontitis and gavaged to C57BL/6 mice. Periodontitis colitis was induced by DSS for 5 d and ligature for 1 wk. The degree of colon inflammation was evaluated through hematoxylin and eosin staining, ELISA, and quantitative real-time polymerase chain reaction. Immune parameters were measured with quantitative real-time polymerase chain reaction, flow cytometry, and immunofluorescence. The gut microbiota and metabolome analyses were performed via 16S rRNA gene sequencing and liquid chromatography-mass spectrometry. Although no significant colitis-associated phenotypic changes were found under physiologic conditions, periodontitis salivary microbiota exacerbated colitis in a periodontitis colitis model after DSS induction. The immune response more closely resembled the pathology of ulcerative colitis, including aggravated macrophage M2 polarization and Th2 cell induction (T helper 2). Inflammatory bowel disease-associated microbiota, such as Blautia, Helicobacter, and Ruminococcus, were changed in DSS-induced colitis after periodontitis salivary microbiota gavage. Periodontitis salivary microbiota decreased unsaturated fatty acid levels and increased arachidonic acid metabolism in DSS-induced colitis, which was positively correlated with Aerococcus and Ruminococcus, suggesting the key role of these metabolic events and microbes in the exacerbating effect of periodontitis salivary microbiota on experimental colitis. Our study demonstrated that periodontitis contributes to the pathogenesis of colitis through the swallowing of salivary microbiota, confirming the role of periodontitis in systemic disease and providing new insights into the etiology of gastrointestinal inflammatory diseases.

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