While these data suggest that inflammation is sufficient to induce dysbiosis, it is also clear that genetic susceptibility plays a role since T. gondii induced heightened dysbiosis and AIEC invasion in mice lacking the ileitis susceptibility gene NOD2, while disease was significantly muted in mice lacking the proinflammatory C-C chemokine receptor 2 (CCR2), which are a model of ileitis resistance (58). This evidence concerns the gene NOD2 and Crohn ileitis.