25,26 Mice deficient for IL-10 have elevated basal expression of IL-22, which reduces acute disease severity following C. difficile infection; however, sustained aberrant inflammation in the context of IL-10 deficiency leads to dysbiosis and increased susceptibility to colitis.27–29 Thus, identifying ways to transiently target IL-22 production may help mitigate the burden of C. difficile infection. This evidence concerns the gene IL10 and colitis.