Antibiotic Effects on Inflammatory Bowel Disease Dynamics

Antibiotics exert a profound influence on the course of inflammatory bowel disease (IBD) by reshaping the intestinal microbiota, modulating mucosal immunity and altering barrier integrity. Broad-spectrum agents can suppress pathogenic bacteria and reduce acute inflammation, yet they may also deplete key commensals that produce protective metabolites such as short-chain fatty acids. Timing and spectrum of antibiotic exposure are critical: early-life courses can induce long-lasting perturbations in microbial composition and immune cell development, increasing susceptibility to later colitis. In established IBD, targeted regimens or adjunctive antimicrobial peptides have shown potential to restore equilibrium between regulatory and pro-inflammatory T-cell subsets, enhance epithelial repair and recalibrate microbial communities. Conversely, indiscriminate antibiotic use may provoke dysbiosis, compromise epithelial barrier function and perpetuate chronic inflammation. Understanding how specific antibiotics, dosages and treatment windows intersect with host–microbe interactions is essential for optimising therapeutic strategies that balance microbial control with preservation of intestinal resilience.

Research from Nature Portfolio

Recent studies have uncovered how selected commensal bacteria can counteract antibiotic-induced dysbiosis and drive immunological tolerance in colitis models. Work using murine and germ-free systems demonstrated that a previously understudied bacterium produces L-lysine-activated short-chain fatty acids which engage the aryl hydrocarbon receptor–indoleamine-2,3-dioxygenase metabolic axis. This mechanism rebalances regulatory T-cell and T helper 17 responses, mitigates mucosal barrier injury and offers a blueprint for metabolite-based adjuncts to conventional antibiotic therapy.

Antibiotic Effects on Inflammatory Bowel Disease Dynamics publication trend

The graph below shows the total number of articles in antibiotic effects on inflammatory bowel disease dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Dysbiosis: Imbalance in the composition or function of the gut microbial community undermining intestinal health.

Short-chain fatty acids: Microbial metabolites (eg, acetate, propionate, butyrate) that support epithelial energy metabolism and regulate immune responses.

Treg/Th17 cells: Subsets of CD4+ T lymphocytes; regulatory T cells (Treg) suppress inflammation while T helper 17 (Th17) cells promote defence against pathogens and can drive tissue damage.

Dextran sulfate sodium (DSS)–induced colitis: A widely used experimental model of acute colonic inflammation in rodents created by administering DSS in drinking water.

Faecal microbiota transplantation (FMT): Transfer of stool from a healthy donor into the gastrointestinal tract of a recipient to restore microbial balance.

References

1. Dubosiella newyorkensis modulates immune tolerance in colitis via the L-lysine-activated AhR-IDO1-Kyn pathway. Nature Communications (2024).
2. Antimicrobial peptide DP7 alleviates dextran sulfate sodium (DSS)‐induced colitis via modifying gut microbiota and regulating intestinal barrier function. MedComm (2025).
3. A single early-in-life antibiotic course increases susceptibility to DSS-induced colitis. Genome Medicine (2020).
4. Perinatal and Antibiotic Exposures and the Risk of Developing Childhood-Onset Inflammatory Bowel Disease: A Nested Case-Control Study Based on a Population-Based Birth Cohort. International Journal of Environmental Research and Public Health (2020).