The reduction of dextran sulfate sodium-induced colitis severity in mice exposed to cigarette smoke is accompanied by specific gene pathway and microbial shifts
Background and aimsThe impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and pre-clinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn's disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition.MethodsThree groups of mice were exposed to three different concentrations of cigarette smoke for a total of four weeks, including five days of dextran sulfate sodium treatment to induce colitis and a seven-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed.ResultsCigarette smoke exposure significantly decreased the severity of induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery.