Background The correlation between periodontitis and ulcerative colitis (UC) has drawn widespread attention recently. Fusobacterium nucleatum (F. nucleatum) as a periodontal pathogen also has reservoirs in gut and may play a role in intestinal diseases. However, its role in the pathogenesis of UC is unclear. Methods Mice were orally given dextran sulphate sodium (DSS) solution and F. nucleatum to construct experimental models. The survival rate, weight, and disease activity index (DAI) of mice were monitored. Alveolar bone loss, abundance of F. nucleatum in colon, colon length, histopathological assessment, and inflammatory cytokines were detected. Apoptosis of intestinal epithelial cells (IECs) were evaluated by TUNEL assay and pro‐apoptotic gene Bax. The epithelial barrier function was assessed by tight junction proteins. By 16S rRNA gene sequencing and LC‐MS‐based methods, the composition of the intestinal microbiota and metabolites in mice were analyzed. Results F. nucleatum facilitated alveolar bone loss and colonized only in infected colon tissue. Mice fed with DSS showed destruction of gut structure, increased expressions of interleukin one‐beta (IL‐1β) and tumor necrosis factor alpha (TNF‐α), decreased expression of IL‐10, higher apoptosis of IECs, microbiota dysbiosis and bile acid dysmetabolism compared to healthy ones. F. nucleatum further aggravated intestinal inflammation and epithelial barrier damage. Probiotics such as Bifidobacterium and Faecalibacterium decreased, opportunistic pathogens Escherichia‐Shigella increased and the differential microorganisms highly associated with inflammatory parameters and metabolites. Meanwhile, level of uric acid involving in the purine metabolism significantly elevated compared to UC mice. Conclusions F. nucleatum promotes gut inflammation, epithelial barrier dysfunction, microbiota dysbiosis and dysmetabolism to aggravate UC.

BackgroundThis study investigated the prevalence and relative abundance of Entamoeba gingivalis (E. gingivalis) in Chinese young patients with different periodontal conditions, and its association with subgingival microbial composition, periodontal parameters, and cytokines in gingival crevicular fluid.MethodsParticipants (age: 18–45 years) diagnosed with stage II–IV periodontitis, gingivitis, or periodontal health underwent periodontal examination and sampling. Subgingival plaque was analyzed by 16S+18S sequencing for E. gingivalis detection and microbial analysis. The distribution of E. gingivalis in subgingival plaque was illustrated by fluorescence in situ hybridization. Interleukin-1β, interleukin-8, and tumor necrosis factor-α in gingival crevicular fluid were measured by multiplexed flow cytometric assay.ResultsThis cross-sectional study included 120 sites from 60 participants. The prevalence and relative abundance of E. gingivalis were significantly increased in periodontitis (p<0.05). The sites were classified into three subgroups according to the relative abundance of E. gingivalis: negative group (Eg0, n=56); low-abundance group (Eg1, n=32); and high-abundance group (Eg2, n=32). The subgingival microflora in the subgroups showed stepwise changes at both the phylum and genus levels. The microflora compositions were significantly altered from Eg0 to Eg2 (p<0.001). Co-occurrence network analysis showed that Porphyromonas, Treponema, Tannerella, Filifactor, TG5, and Desulfobulbus were highly correlated with E. gingivalis (r>0.6, p<0.001). Correlation analysis showed that E. gingivalis was closely associated with important periodontal parameters and cytokines (p<0.01).ConclusionE. gingivalis was enriched in periodontitis and closely associated with subgingival microbial dysbiosis, periodontal parameters and cytokines in gingival crevicular fluid. Thus, it may be an important pathogen in periodontal disease.