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特应性皮炎患者皮肤中的类二十烷酸:前列腺素E2和白三烯B4以生物活性浓度存在。

Eicosanoids in skin of patients with atopic dermatitis: prostaglandin E2 and leukotriene B4 are present in biologically active concentrations.

作者信息

Fogh K, Herlin T, Kragballe K

机构信息

Department of Dermatology, University of Aarhus, Denmark.

出版信息

J Allergy Clin Immunol. 1989 Feb;83(2 Pt 1):450-5. doi: 10.1016/0091-6749(89)90132-2.

Abstract

The biochemical events leading to atopic dermatitis (AD) are unknown. Certain eicosanoids derived from arachidonic acid are potent mediators of skin inflammation and modulators of certain T-lymphocyte activities. The purpose of the present study was to determine whether eicosanoids are present in biologically active concentrations in the skin of adult patients with AD. The levels of the cyclooxygenase product, prostaglandin E2 (PGE2) and the lipoxygenase products, leukotriene B4 (LTB4), 12- and 15-hydroxyeicosatetraenoic acid were determined in biopsy specimens obtained by keratome from lesional, perilesional, and clinically unaffected skin of patients with AD. Methods for identification of eicosanoids included reversed-phase high-performance liquid chromatography combined with radioimmunoassays. Eicosanoid levels were at the same level in normal skin and in uninvolved skin of AD. Compared with uninvolved skin, both lesional and perilesional skin contained markedly elevated concentrations of PGE2 and LTB4: PGE2, 97.2 +/- 15.6 ng/gm of lesional skin and 128.3 +/- 27.2 ng/gm of perilesional skin; LTB4, 5.2 +/- 1.6 ng/gm of lesional skin and 3.2 +/- 0.6 ng/gm of perilesional skin. Compared with uninvolved skin, the levels of 12- and 15-hydroxyeicosatetraenoic acid were elevated sevenfold and elevenfold, respectively, in lesional skin, but did not reach biologically active concentrations. The results demonstrate that the inflammatory mediators PGE2 and LTB4 are present in lesional skin of atopic subjects in biologically active concentrations. Because these mediators are able to induce cutaneous inflammation and to modulate cellular immunity, they may be involved in the biochemical processes leading to AD.

摘要

导致特应性皮炎(AD)的生化事件尚不清楚。某些由花生四烯酸衍生的类二十烷酸是皮肤炎症的强效介质和某些T淋巴细胞活性的调节剂。本研究的目的是确定类二十烷酸是否以生物活性浓度存在于成年AD患者的皮肤中。通过角膜刀从AD患者的皮损、皮损周围和临床未受累皮肤获取活检标本,测定环氧化酶产物前列腺素E2(PGE2)以及脂氧合酶产物白三烯B4(LTB4)、12-和15-羟基二十碳四烯酸的水平。类二十烷酸的鉴定方法包括反相高效液相色谱结合放射免疫测定。正常皮肤和AD未受累皮肤中的类二十烷酸水平相同。与未受累皮肤相比,皮损和皮损周围皮肤中PGE2和LTB4的浓度均显著升高:PGE2,皮损皮肤中为97.2±15.6 ng/gm,皮损周围皮肤中为128.3±27.2 ng/gm;LTB4,皮损皮肤中为5.2±1.6 ng/gm,皮损周围皮肤中为3.2±0.6 ng/gm。与未受累皮肤相比,皮损皮肤中12-和15-羟基二十碳四烯酸的水平分别升高了7倍和11倍,但未达到生物活性浓度。结果表明,炎症介质PGE2和LTB4以生物活性浓度存在于特应性受试者的皮损皮肤中。由于这些介质能够诱导皮肤炎症并调节细胞免疫,它们可能参与了导致AD的生化过程。

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