Disturbances of essential fatty acid- and prostaglandin E-mediated immunoregulation in atopy.
Impaired suppressor T lymphocyte maturation and function in atopic individuals are explained by an insufficient transmission of prostaglandin E (PGE) signals during thymic lymphocyte differentiation as well as an impaired ability of the atopic immune system to activate suppressor T-cells by PGE-mediated feed back mechanisms. We demonstrate that spontaneous in vitro immunoglobulin E synthesis of atopic peripheral blood mononuclear cells could be suppressed by the addition of 10(-6) M to 10(-5) M PGE1 or PGE2. Decreased plasma and breast milk levels of PGE-precursor fatty acids and reduced numbers of PGE2-receptors on atopic lymphocytes have been observed in atopic individuals. These insights might offer a novel approach for the prevention of atopic disease by substitution of the atopic pregnant and nursing woman and her newborn infant with long chain omega-6-fatty acids.
Melnik
B C
BC
Department of Dermatology, Heinrich-Heine-University of Düsseldorf, Germany.
Plewig
G
G
Tschung
T
T
D000328:Adult; D000527:Alprostadil / Q000494:pharmacology; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology; D005228:Fatty Acids, Essential / Q000172:deficiency / Q000276:immunology* / Q000378:metabolism; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D066298:In Vitro Techniques; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008895:Milk, Human / Q000276:immunology / Q000378:metabolism; D011247:Pregnancy; D011458:Prostaglandins E / Q000276:immunology* / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology
D005228:Fatty Acids, Essential; D011458:Prostaglandins E; D007073:Immunoglobulin E; D000527:Alprostadil; D015232:Dinoprostone