Mechanism Of Periodontitis Aggravating Ulcerative Colitis Through Gut Microbiota

To investigate the impact of periodontitis on ulcerative colitis (UC) severity and to explore the underlying mechanisms preliminarily. A total of 20 male C57BL/6J mice were randomly assigned to four groups: Sham, Periodontitis (P), UC, and Periodontitis - UC (P-UC). A chronic UC model was induced by alternating oral administration of 1% and 0.5% Dextran Sulfate Sodium Salt (DSS) solution, while periodontitis was induced by ligatures. The severity of periodontitis on UC was evaluated through the DAI score, histopathological analysis of colon tissue, and evaluation of intestinal permeability. The gut microbiota was analyzed using 16S rRNA sequencing. TNF-α, IL-6 etc. were measured by qPCR to evaluate the systemic inflammation burden. ZO-1, occludin etc. were assessed using qPCR and immunohistochemistry. Compared to the UC group, the P-UC group exhibited greater colonic inflammation, with significantly elevated mRNA expression levels of TNF-α and IL-6 in intestinal tissues (P<0.0001, P<0.05). Additionally, the P-UC group demonstrated altered intestinal barrier function, with increased ZO-1 mRNA levels (P<0.01), though protein levels were decreased. Both the P-UC and UC groups exhibited notable dysbiosis of the gut microbiota, with the P-UC group showing significantly higher abundance of UC-associated bacteria, such as Muribaculum and Allobaculum (P<0.05), compared to the UC group. Periodontitis may exacerbate UC by increasing the abundance of harmful gut bacteria, and promoting the secretion of pro-inflammatory cytokines, thereby disrupting the intestinal barrier and worsening UC severity.