In natural T. gondii infection through the oral route, exacerbated inflammatory responses at the small intestine (ileitis) resemble human inflammatory bowel disease (IBD) [1], [7].The inflammatory response coordinate by IL-23/IL-22 is involved in T. gondii-induced disruption of intestinal homeostasis and immunopathology, an effect at least in part due to increase expression of matrix metalloproteinase-2 (MMP) [7]. This evidence concerns the gene MMP2 and Crohn ileitis.