ABSTRACT
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 prostaglandin E1 (PGE1) or PGE2. 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. Decreased levels of 6-desaturated PGE-precursor fatty acids in plasma, T lymphocytes, monocytes, adipose tissue and breast milk have been observed in atopic individuals. These insights might offer a novel approach to 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.
Subject(s)
Dermatitis, Atopic/immunology , Immunoglobulin E/biosynthesis , Monocytes/immunology , Prostaglandins E/deficiency , Cells, Cultured , Dermatitis, Atopic/prevention & control , Female , Humans , Immunity, Cellular , Pregnancy , Prostaglandins E/immunology , T-Lymphocytes/immunologyABSTRACT
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.
Subject(s)
Dermatitis, Atopic/immunology , Fatty Acids, Essential/immunology , Prostaglandins E/immunology , Adult , Alprostadil/pharmacology , Dermatitis, Atopic/metabolism , Dinoprostone/pharmacology , Fatty Acids, Essential/deficiency , Fatty Acids, Essential/metabolism , Female , Humans , Immunoglobulin E/biosynthesis , In Vitro Techniques , Leukocytes, Mononuclear/drug effects , Leukocytes, Mononuclear/immunology , Leukocytes, Mononuclear/metabolism , Milk, Human/immunology , Milk, Human/metabolism , Pregnancy , Prostaglandins E/metabolism , T-Lymphocytes, Regulatory/drug effects , T-Lymphocytes, Regulatory/immunologyABSTRACT
From L-serine 2-(linoleoylamino)-1,3-propanediol, a monoglyceride analogue, was synthesized and characterized by thin-layer and gas chromatography, infra red spectroscopy and mass spectrometry. After oral application to rats there was an accumulation, almost exclusively in the liver, of triglyceride, diglyceride, phosphatidylcholine and phosphatidylethanolamine analogues with amide-bound linoleic acid. Small amounts of triglyceride analogues could also be detected in the adipose tissue. The analogues were chromatographically isolated using in addition enzymatic and non-enzymatic hydrolysis procedures. Results disclosed that the amide-bound fatty acid of 2-(linoleoylamino)-1,3-propanediol can be absorbed and metabolized intact. Phosphoglyceride analogues are probably formed by the CDP-choline and CDP-ethanolamine pathway fromdiglyceride analogues. Phosphatidylcholine and its analogues disclosed a similar composition of the 1-O-acyl fatty acids. Apparently analogues have in vivo similar substrate properties to hydrolases and acyltransferases as their natural counterparts.
