The potential contribution of microbial translocation to SBM-induced enteritis was reinforced by the substantial up-regulation of the IFNG transcript and the enrichment of associated pathways (e.g., role of PKR in interferon induction and antiviral response) as well as modification of pathways directly linked to the intestinal barrier function and permeability (e.g., remodeling of epithelial adherens junctions and epithelial adherens junction signalling). Here, IFNG is linked to enteritis.