Treatment with TNBS induced colitis with increased tissue damage, inflammation, gut dysbiosis as seen with increase in Betaproteobacteria and Actinobacteria, decreased goblet cells and endocytic function. Treatment with acetic, propionic, and butyric acid (SCFAs) reduced expression of inflammatory cytokines (il1b and il6), recruitment of neutrophils in the intestinal, maintained bacterial population level in gut comparable to control, but did not restore tissue damage in intestinal wall or number of goblet cells. The gene discussed is IL1B; the disease is colitis.