Abstract
ω3 polyunsaturated fatty acids (PUFAs) have anti-allergic and anti-inflammatory properties, but the immune-metabolic progression from dietary oil remains to be investigated. Here we identified 17,18-epoxyeicostetraenoic acid (17,18-EpETE) as an anti-allergic metabolite generated in the gut from dietary ω3 α-linolenic acid (ALA). Biochemical and imaging mass spectrometry analyses revealed increased ALA and its metabolites, especially eicosapentaenoic acid (EPA), in the intestines of mice receiving ALA-rich linseed oil (Lin-mice). In murine food allergy model, the decreased incidence of allergic diarrhea in Lin-mice was due to impairment of mast cell degranulation without affecting allergen-specific serum IgE. Liquid chromatography–tandem mass spectrometry-based mediator lipidomics identified 17,18-EpETE as a major ω3 EPA-derived metabolite generated from dietary ALA in the gut, and 17,18-EpETE exhibits anti-allergic function when administered in vivo. These findings suggest that metabolizing dietary ω3 PUFAs generates 17,18-EpETE, which is an endogenous anti-allergic metabolite and potentially is a therapeutic target to control intestinal allergies.
Highlights
V3 polyunsaturated fatty acids (PUFAs) have anti-allergic and anti-inflammatory properties, but the immune-metabolic progression from dietary oil remains to be investigated
Because v3 and v6 PUFAs compete in metabolic pathways[18], increased v3 PUFA and decreased v6 PUFA intake reduces the onset of aberrant murine and human immunologic conditions, including food allergy[19,20,21]; the effector lipid metabolites from the dietary oils to the regulation of food allergy are unknown
Dietary v3 a-linolenic acid (ALA)-enriched linseed oil prevents the development of allergic diarrhea by preventing effector phases of intestinal allergy
Summary
V3 polyunsaturated fatty acids (PUFAs) have anti-allergic and anti-inflammatory properties, but the immune-metabolic progression from dietary oil remains to be investigated. Liquid chromatography– tandem mass spectrometry-based mediator lipidomics identified 17,18-EpETE as a major v3 EPA-derived metabolite generated from dietary ALA in the gut, and 17,18-EpETE exhibits anti-allergic function when administered in vivo. These findings suggest that metabolizing dietary v3 PUFAs generates 17,18-EpETE, which is an endogenous anti-allergic metabolite and potentially is a therapeutic target to control intestinal allergies. The immunologic mechanisms in the development of food allergy involve the disruption of oral tolerance, induction of Th2-type responses, allergen-specific IgE production, and mast cell (MC) activation[2,3] These immune responses have been studied in several murine models of food allergy (including ours)[4,5,6,7,8]. We identified v3 EPA-derived metabolite derived from dietary ALA in the gut, which is a promising candidate for the prevention of intestinal allergy
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