Specifically, in mouse studies, IL-22 has been shown (i) to direct glycosylation of the gut microbiome, creating an unfavorable environment for Clostrioides difficile; (ii) reduce CDI-mediated colonic inflammation; (iii) limit the negative consequences of systemic dissemination of commensal bacteria through complement-activated bacterial phagocytosis; and (iv) improve morbidity and mortality associated with infection (34, –, 36). Here, IL22 is linked to clostridium difficile infection.