Omega‐3 fatty acids protect from colitis via an Alox15‐derived eicosanoid

An increased omega-3 polyunsaturated fatty acid (n-3 PUFA) tissue status can lead to a significant formation of anti-inflammatory lipid mediators and effective reduction in inflammation injury murine colitis. Arachidonic lipoxygenases (ALOX) have been implicated the pathogenesis inflammatory bowel disease as well pro- mediators. To explore role Alox15 protective response found fat1 transgenic mice with endogenously n-3 PUFA were crossed Alox15-deficient animals challenged dextran sulfate sodium (DSS)- 2,4,6-trinitrobenzene sulphonic (TNBS)-induced colitis model. Transgenic rich endogenous PUFAs protected from However, additional systemic inactivation gene counteracted this effect. molecular basis for effect metabolites derived analyzed different mice. deficiency suppressed PUFA-derived 15-hydroxy eicosapentaenoic (15-HEPE). In contrast, treating intraperitoneal injections 15S-HEPE wild-type DSS- TNBS-induced These data suggest that anti-colitis mouse model is mediated part via Alox15-derived 15-HEPE formation.