IL1B and clostridium difficile infection: Acetate–FFAR2 interaction activated the inflammasome that resulted in the release of IL-1β and further promoted the secretion of IL-22 in ILC3 through IL-1 receptor signaling in response to IL-1β (Figure 2).47 In the mouse CDI model, secretion of IL-22 cytokine was induced and the IL-22-/- KO mice showed increased pathobiont load and resistance to complement mediated phagocytosis.105 Administration of IL-22 helped clear the pathobiont load by increased phagocytosis.