Consumption of a baked corn and bean snack reduced chronic colitis inflammation in CD-1 mice via downregulation of IL-1 receptor, TLR, and TNF-α associated pathways

Ulcerative colitis (UC) is a condition that has been rising in the number of cases around the world. Food products made from natural ingredients such as corn and common bean might serve as alternatives for the treatment of UC. This study aimed to assess the anti-inflammatory effect of the consumption of a baked corn and bean snack (CBS) in an in vivo model of UC using 2% dextran sodium sulfate (DSS) as inductor of colitis. CD-1 mice (45, n = 9/group) were randomly separated into 5 groups, treated for 6-weeks as follows: G1 (basal diet, BD), G2 (2% DSS), G3 (20 g CBS/body weight BW/day + BD), G4 (40 g CBS/BW/day + BD) and G5 (60 g CBS/BW/day + BD). BW, Disease Activity Index (DAI), and feces were collected throughout the treatment. After euthanasia, organs (spleen, liver, and colon) were excised and weighed. Feces were analyzed for β-glucuronidase (β-GLUC) activity and gas-chromatography. The colons were analyzed for histopathology, myeloperoxidase (MPO) activity, and gene analysis. At the end of treatments, among the DSS-induced groups, G3 exhibited the lowest BW losses (11.5%), MPO activity (10.4%) and β-GLUC (8.6%). G4 presented the lowest DAI (0.88), relative spleen weight, and histological inflammation score (p < 0.05). Compared to G2, CBS consumption significantly (p < 0.05) reduced serum TNF-α, IL-10, and MCP-1 levels. The fecal metabolome analysis ranked 9-decenoic acid, decane, and butyric acid as the main contributors of pathways associated with the β-oxidation of fatty acids. G4 showed the highest fecal/cecal contents of short-chain fatty acids among all the DSS-induced groups. For the gene expression, G4 was clustered with G1, showing a differential inhibition of the pro-inflammatory genes Il1r1, Il1a, Tlr4, Tlr2, and Tnfrsf1b. In conclusion, CBS consumption decreased the inflammatory state and reduced the expression of the IL-1 receptor, TLR, and TNF-α-associated pathways in DSS-induced UC in CD-1 mice.