Is the origin of atopy linked to deficient conversion of omega-6-fatty acids to prostaglandin E1?
Our hypothesis on the origin of atopy links alterations in omega-6-fatty acid metabolism in atopic persons (i.e., reduced formation of delta-6-desaturase products) to deficient T cell differentiation and function. We suggest that a relative deficiency in dihomo-gamma-linolenic acid-derived prostaglandin E1 is the major etiologic factor for diminished T cell maturation postpartum. Its precursors, gamma-linolenic acid and dihomo-gamma-linolenic acid, are physiologically provided in colostrum and mature breast milk of healthy mothers. Depressed cell-mediated immunity and uncontrolled B-cell response with increased IgE synthesis are explained as prostaglandin E1-dependent defects of T cell differentiation caused by insufficient supply of prostaglandin E1 precursors during early infancy. Thus, in our opinion atopy is a metabolic disorder and the associated immunologic disturbances are epiphenomena.
Melnik
B C
BC
Department of Dermatology, University of Düsseldorf, F.R.G.
Plewig
G
G
D000276:Adjuvants, Immunologic / Q000502:physiology; D000527:Alprostadil / Q000378:metabolism* / Q000502:physiology; D001942:Breast Feeding; D002454:Cell Differentiation; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000378:metabolism; D044943:Fatty Acid Desaturases / Q000172:deficiency; D006801:Humans; D008042:Linolenic Acids / Q000378:metabolism* / Q000502:physiology; D050602:Linoleoyl-CoA Desaturase; D013601:T-Lymphocytes / Q000166:cytology; D017965:gamma-Linolenic Acid
D000276:Adjuvants, Immunologic; D008042:Linolenic Acids; D017965:gamma-Linolenic Acid; D044943:Fatty Acid Desaturases; D050602:Linoleoyl-CoA Desaturase; D000527:Alprostadil