Consequentially, signaling via these pro-inflammatory cytokines has been shown to exacerbate IBD-associated pathology in response to infection with Helicobacter typhlonius and in mouse models of dextran sulfate sodium (DSS)-induced colitis (12, 25, 43, 55, 57–59)—for example, in response to DSS treatment, IFN-γ disrupts the vascular barrier integrity by altering the adherens junction protein VE-cadherin. The gene discussed is IFNG; the disease is colitis.