In an animal model of colitis, they improved barrier function by reducing the levels of TNF-α, IL-6, IL-1β, IL-17, and other cytokines, upregulating the levels of intestinal barrier markers claudin-1 and ZO-1, increasing Lactobacillus abundance, and inhibiting Bacteroides abundance, thereby restoring gut microbiota composition and alleviating experimental colitis in mice [58]. This evidence concerns the gene IL17A and colitis.