IL-17A has been shown to be a protective mediator during CDI; its reduction induced by pretreatment with the S100B inhibitor may be a result of the downregulation of pro-inflammatory mediators such as IL-1β and IL-23, both of which are known as inductors of this cytokine (Shibata et al., 2007; Sutton et al., 2009). Here, S100B is linked to clostridium difficile infection.