Ant may well destroy a whole dam: glycans of colonic mucus barrier disintegrated by gut bacteria.

The colonic mucus layer plays a critical role in maintaining the integrity of the colonic mucosal barrier, serving as the primary defense against colonic microorganisms. Predominantly composed of mucin 2 (MUC2), a glycosylation-rich protein, the mucus layer forms a gel-like coating that covers the colonic epithelium surface. This layer provides a habitat for intestinal microorganisms, which can utilize mucin glycans present in the mucus layer as a sustainable source of nutrients. Additionally, metabolites produced by the microbiota during the metabolism of mucus glycans have a profound impact on host health. Under normal conditions, the production and consumption of mucus maintain a dynamic balance. However, several studies have demonstrated that certain factors, such as dietary fiber deficiency, can enhance the metabolism of mucus glycans by gut bacteria, thereby disturbing this balance and weakening the mucus barrier function of the mucus layer. To better understand the occurrence and development of colon-related diseases, it is crucial to investigate the complex metabolic patterns of mucus glycosylation by intestinal microorganisms. Our objective was to comprehensively review these patterns in order to clarify the effects of mucus layer glycan metabolism by intestinal microorganisms on the host.

Association between inflammatory bowel disease and periodontitis: A bidirectional two-sample Mendelian randomization study.

AIM: This Mendelian randomization (MR) study was performed to explore the potential bidirectional causal association between inflammatory bowel disease (IBD) and periodontitis. MATERIALS AND METHODS: We used genetic instruments from the genome-wide association study summary statistics of European descent for IBD (12,882 cases and 21,770 controls) to investigate the association with periodontitis (3046 cases and 195,395 controls) and vice versa. The radial inverse-variance weighted method was carried out to obtain the primary causal estimates, and the robustness of the results was assessed by a series of sensitivity analyses. Due to multiple testing, associations with p values <.008 were considered as statistically significant, and p values ≥.008 and <.05 were considered as suggestively significant. RESULTS: In the primary causal estimates, IBD as a whole was associated with an increased risk of periodontitis (odds ratio [OR], 1.060; 95% confidence interval [CI], 1.017; 1.105; p = .006). Subtype analyses showed that ulcerative colitis (UC) was associated with periodontitis (OR, 1.074; 95% CI 1.029; 1.122; p = .001), while Crohn's disease (CD) was not. Regarding the reverse direction, periodontitis showed a suggestive association with IBD as a whole (OR, 1.065; 95% CI 1.013; 1.119; p = .014). Subtype analyses revealed that periodontitis was associated with CD (OR, 1.100; 95% CI 1.038; 1.167; p = .001) but not UC. The final models after outlier removal showed no obvious pleiotropy, indicating that our primary analysis results were reliable. CONCLUSIONS: The present MR study provides moderate evidence on the bidirectional causal relationship between IBD and periodontitis. The bidirectional increased risk found in our study was marginal and, possibly, of limited clinical relevance. More studies are needed to support the findings of our current study.