Chung K F
National Heart and Lung Institute, Imperial College London, London SW3 6LY, UK.
Sci STKE. 2005 Sep 27;2005(303):pe47. doi: 10.1126/stke.3032005pe47.
Prostaglandin E2 (PGE2) released in asthmatic airways has bronchodilator properties and inhibits allergen-induced bronchoconstriction and release of inflammatory mediators. Although considered as a potential treatment for asthma, PGE2 also has some proinflammatory properties. PGE2 acts through four different receptor subtypes (EP1, EP2, EP3, and EP4) that may explain some of PGE2's diverse effects. In a mouse model of allergic inflammation in which the four receptors were individually deleted, only EP3(-/-) mice showed an enhancement of inflammation, whereas an EP3 agonist was inhibitory, with PGE2 being inactive. Thus, EP3 agonists may lead to a new approach for the treatment of asthma. However, other PGE2 receptor subtypes may also have beneficial effects, and a greater understanding of the signaling pathways of these receptor subtypes will help to clarify the role of these receptors in asthma.
哮喘气道中释放的前列腺素E2（PGE2）具有支气管扩张特性，可抑制变应原诱导的支气管收缩和炎症介质释放。尽管PGE2被视为哮喘的一种潜在治疗方法，但它也具有一些促炎特性。PGE2通过四种不同的受体亚型（EP1、EP2、EP3和EP4）发挥作用，这可能解释了PGE2的一些不同效应。在一种过敏性炎症小鼠模型中，这四种受体被分别敲除，只有EP3基因敲除（EP3(-/-)）小鼠表现出炎症增强，而EP3激动剂具有抑制作用，PGE2则无活性。因此，EP3激动剂可能为哮喘治疗带来新方法。然而，其他PGE2受体亚型可能也具有有益作用，更深入了解这些受体亚型的信号通路将有助于阐明这些受体在哮喘中的作用。
