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细胞外哺乳动物14 kDa II组磷脂酶A2介导抗原致敏肥大细胞生成类二十烷酸。

Eicosanoid generation from antigen-primed mast cells by extracellular mammalian 14-kDa group II phospholipase A2.

作者信息

Murakami M, Kudo I, Inoue K

机构信息

Department of Health Chemistry, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.

出版信息

FEBS Lett. 1991 Dec 9;294(3):247-51. doi: 10.1016/0014-5793(91)81440-j.

DOI:10.1016/0014-5793(91)81440-j
PMID:1756867
Abstract

The extracellular form of 14-kDa group II phospholipase A2 has been found to accumulate at various types of inflammatory sites. In the present paper, we have studied the possible role of the extracellular 14-kDa group II phospholipase A2 in the process of prostaglandin production in activated rat mast cells. When mast cells obtained from the peritoneal cavity of rats were sensitized with IgE, challenged with antigen and then exposed to extracellular 14-kDa group II phospholipase A2, appreciable release of prostaglandin D2 was observed. Generation of prostaglandin D2 was dependent on the concentration of the phospholipase A2 as well as that of the antigen, while no appreciable prostaglandin D2 generation was observed with cells in the absence of the antigen. No histamine release was observed under the same conditions. Phosphatidylcholine in mast cell membranes was appreciably hydrolyzed to liberate free arachidonic acid when mast cells were incubated with 14-kDa group II phospholipase A2 added exogenously in the presence of the antigen. Both the generation of prostaglandin D2 and the release of arachidonic acid were retarded by inhibitors specific to 14-kDa group II phospholipase A2. Thus, 14-kDa group II phospholipase A2 may function in the process of inflammation by acting on IgE-antigen-primed mast cells, which are not fully activated, to generate eicosanoids.

摘要

已发现14 kDa II型磷脂酶A2的细胞外形式在各种类型的炎症部位积累。在本文中,我们研究了细胞外14 kDa II型磷脂酶A2在活化的大鼠肥大细胞中前列腺素产生过程中的可能作用。当用IgE使从大鼠腹腔获得的肥大细胞致敏,用抗原攻击然后暴露于细胞外14 kDa II型磷脂酶A2时,观察到前列腺素D2有明显释放。前列腺素D2的产生取决于磷脂酶A2的浓度以及抗原的浓度,而在无抗原的情况下,细胞未观察到明显的前列腺素D2产生。在相同条件下未观察到组胺释放。当肥大细胞在抗原存在下与外源添加的14 kDa II型磷脂酶A2一起孵育时,肥大细胞膜中的磷脂酰胆碱明显水解以释放游离花生四烯酸。前列腺素D2的产生和花生四烯酸的释放均被14 kDa II型磷脂酶A2特异性抑制剂所抑制。因此,14 kDa II型磷脂酶A2可能通过作用于未完全活化的IgE-抗原致敏肥大细胞来产生类花生酸,从而在炎症过程中发挥作用。

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