Lipoxins: putative braking signals in host defense, inflammation and hypersensitivity.
Lipoxins: putative braking signals in host defense, inflammation and hypersensitivity.
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DOI：
10.1097/00041552-199601000-00006
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发表时间：
1996-01-01
影响因子：
3.2
通讯作者：
Serhan, C N
中科院分区：
文献类型：
--
作者：
Brady, H R;Serhan, C N
脂氧素是花生四烯酸衍生的脂质介质，其在结构和功能上与其他类花生酸不同。它们是通过跨细胞途径产生的，该途径最初涉及花生四烯酸通过15-和5-脂氧合酶或通过5-和1.2-脂氧合酶（脂氧合酶相互作用产物）的双重脂氧合。血小板-中性粒细胞相互作用是血管腔内脂氧素的特别丰富的来源。细胞-细胞粘附和细胞因子是这些复杂的生物合成回路的重要放大器。白细胞和内皮细胞表达脂氧素的高亲和力受体，其参与引起信号转导事件和生物活性的独特特征。在许多测定系统中，脂氧素阻止由白三烯和其他介质诱导的嗜中性粒细胞的趋化性、粘附和迁移，表明脂氧素可能在宿主防御、炎症和超敏反应中充当内源性制动信号。有趣的是，环加氧酶II，在阿司匹林的存在下，催化形成一个新的系列的15-epi-lipoxins在嗜中性粒细胞-内皮细胞的相互作用，这表明一个新的机制，这种常用的治疗剂的作用。
Lipoxins are arachidonate-derived lipid mediators that are structurally and functionally distinct from other classes of eicosanoids. They are generated via transcellular pathways that initially involve the dual lipoxygenation of arachidonic acid either by 15- and 5-lipoxygenases or by 5- and 1.2-lipoxygenases (lipoxygenase interaction products). Platelet-neutrophil interactions are a particularly rich source of lipoxins within the vascular lumen. Cell-cell adhesion and cytokines are important amplifiers of these complex biosynthetic circuits. Leukocytes and endothelial cells express high affinity receptors for lipoxins, engagement of which evokes a unique profile of signal transduction events and bioactivities. In many assay systems, lipoxins prevent chemotaxis, adhesion, and transmigration of neutrophils induced by leukotrienes and other mediators, suggesting that lipoxins may act as endogenous braking signals in host defense, inflammation, and hypersensitivity reactions. Intriguingly, cyclo-oxygenase II, in the presence of aspirin, catalyses the formation of a novel series of 15-epi-lipoxins during neutrophil-endothelial cell interactions, suggesting a new mechanism of action for this commonly used therapeutic agent.