The increase in IL-18 secretion observed in CRM12-infected mice likely results from the deletion of NleF, which normally suppresses this cytokine’s processing and secretion.56 This increase combined with the lower tissue damage could make CRM12 a good tool to study the effect of local IL-18 responses in colitis, given its role in intestinal tolerance.57 Similarly, the absence of Map in CRM12 may contribute to the observed milder disruption of gut barrier function.58 This evidence concerns the gene IL18 and colitis.