Eicosanoids in asthma.

K. Wan, Wei-Fong Wu
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引用次数: 8

Abstract

Eicosanoids belong to a diverse family of bioactive fatty acids that play important roles in regulating airway inflammation and reactivity. They are the key mediators of the pathobiology of asthma. Among the eicosanoids, lipoxins (LXs) were the first agents to be identified and recognized as potential anti-inflammatory endogenous lipid mediators. Lipoxins are biosynthesized in vivo at inflammation sites. They result mainly from the interaction between 5 and 15-lipoxygenases (LOs), which are distinct from leukotrienes (LTs) and prostaglandins (PGs) in structure and function. Leukotrienes are potent proinflammatory mediators and directly and indirectly stimulate fibroblast chemotaxis, proliferation, and collagen synthesis. Prostaglandins have both bronchoconstrictive and bronchoprotective effects and the bronchoconstriction mediated by PGD2 and PGF2alpha is only occurred in asthmatic patients but not in healthy subjects. Lipoxins counter-regulate the proinflammatory actions of LTs and activate resolution of the inflammatory response. At least two classes of receptors, CysLT1 receptors and Asprin-triggered lipoxin A4 (ALX) receptors, can interact with lipoxin A4 (LXA4) and LXA4 analogs to mediate their biologic actions. Allergen challenge initiates airway biosynthesis of LXA4 and increases expression of its receptor. In addition, LXA4 affects the release of interleukin-8 by blood mononuclear cells, and ALX affects calcium influx into epithelial cells. Therefore, the pivotal role of LXs is mediating airway homeostasis, and LXs may be part of a novel, multipronged approach for treating human asthma.
哮喘中的类二十烷酸。
类二十烷酸属于多种生物活性脂肪酸家族,在调节气道炎症和反应性方面发挥重要作用。它们是哮喘病理生物学的关键介质。在类二十烷类化合物中,脂毒素(lipoxins, LXs)是最早被发现并被认为是潜在的抗炎内源性脂质介质。脂毒素是在体内炎症部位生物合成的。它们主要是由5-和15-脂氧合酶(LOs)之间的相互作用引起的,它们在结构和功能上不同于白三烯(lt)和前列腺素(pg)。白三烯是有效的促炎介质,直接或间接刺激成纤维细胞趋化、增殖和胶原合成。前列腺素具有支气管收缩和支气管保护作用,PGD2和PGF2alpha介导的支气管收缩仅发生在哮喘患者中,而不发生在健康受试者中。脂质可以抑制LTs的促炎作用,并激活炎症反应的消退。至少有两类受体,CysLT1受体和阿司匹林触发的脂素A4 (ALX)受体,可以与脂素A4 (LXA4)和LXA4类似物相互作用,介导它们的生物作用。过敏原攻击启动气道LXA4的生物合成并增加其受体的表达。此外,LXA4影响血液单核细胞释放白细胞介素-8,ALX影响钙流入上皮细胞。因此,LXs的关键作用是调节气道内稳态,并且LXs可能是治疗人类哮喘的一种新的、多管齐下的方法的一部分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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