AI Article Synopsis
- Th17 cells play a crucial role in the immune response against oral pathogens, particularly in the development of periodontitis.
- The oral pathobiont Porphyromonas gingivalis exacerbates periodontitis by promoting Th17 cell differentiation, which occurs in Peyer's patches and allows these cells to migrate to oral tissues.
- The study shows that the intestinal microbiome influences Th17 cell response, with antibiotic treatment altering the microbiome potentially impacting the progression of periodontitis.
Article Abstract
Host immune response via Th17 cells against oral pathobionts is a key mediator in periodontitis development. However, where and how the Th17-type immune response is induced during the development of periodontitis is not well understood. Here, we demonstrate that gut translocation of the oral pathobiont Porphyromonas gingivalis (Pg) exacerbates oral pathobiont-induced periodontitis with enhanced Th17 cell differentiation. The oral pathobiont-responsive Th17 cells are differentiated in Peyer's patches and translocated systemically in the peripheral immune tissues. They are also capable of migrating to and accumulating in the mouth upon oral infection. Development of periodontitis via the oral pathobiont-responsive Th17 cells is regulated by the intestinal microbiome, and altering the intestinal microbiome composition with antibiotics affects the development of periodontitis. Our study highlights that pathobiont-responsive Th17 cells in the gut-mouth axis and the intestinal microbiome work together to provoke inflammatory oral diseases, including periodontitis.
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| http://dx.doi.org/10.1016/j.celrep.2022.111314 | DOI Listing |
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