PGE2 通过 EP2 受体调控 IgE 型抗体分泌参与哮喘疾病
PGE2 regulates IgE secretion and interfere with the development of asthma through EP2
目的:哮喘,作为一种慢性呼吸道疾病,已经成为了当前世界性的主要导致死亡的原因之一。前列腺素E2(PGE2)是一种极其重要的脂类介质,已被证实在哮喘病人血清中的高浓度表达,并可能在哮喘发生发展中的多个环节发挥重要作用。本文将着力探讨 PGE2 对哮喘疾病的干扰机制。方法:本课题围绕 OVA 诱导的哮喘模型,深入探讨了PGE2 通过其受体 EP2 在哮喘发生中的潜在调节机制。结果:相对诱导成功的野生型小鼠,EP2受体的缺失将大幅降低小鼠哮喘的发病率。EP2 基因敲除小鼠血清中总的IgE水平和OVA特异的 IgE浓度均大幅下降。其呼吸道未出现气道高反应性且其支气管组织的病理改变也得到了相应的缓解。体外实验进一步证明,PGE2 通过其 EP2 和 EP4 受体完成对 B 细胞的调控,从而影响该疾病的发生发展。结论:PGE2 借助 EP2 受体传导的信号能够对 B 细胞 IgE 型抗体分泌产生正向调控,因此并进一步加重了哮喘疾病的发生发展。这为该疾病治疗的提供了新的药物靶点。
im: As chronic respiratory disease, asthma representing severe problems for world public health is currently the major leading cause of death, and it has been proved that elevated prostaglandin E2 (PGE2) concentration can be detected in serum and sputum of patients with asthma, suggesting intimate relationship between these two factors. The aim of current study is to explore the influence of PGE2 on asthma. Methods: Based on the OVA-induced asthma model, the fundemental effect of EP2 deficiency was fully examined in vivo and in vitro. Results: the IgE concentration in serum from EP2 knockout mice(EP2 KO mice) was detected much lower than wildtype. In vitro experiment result suggested that its B cells cannot be stimulated and secreted IgE antibody effecienctly. In vivo study, compared with wild type mice, EP2 knockout mice (EP2 KO mice) had a significantly lower total IgE and OVA-specific IgE in their serum. Moreover, EP2 KO mice didn't have airway hyperresponse as well as the pathological change of their lung tissure was mild. Conclusion: the PGE2-EP2 pathway was an important positive modulator of allergic reactions and IgE production.
张毓、高雨涵、王巍
基础医学内科学
免疫学前列腺素E2EP2哮喘。
ImmunologyPGE2EP2asthma.
张毓,高雨涵,王巍.PGE2 通过 EP2 受体调控 IgE 型抗体分泌参与哮喘疾病[EB/OL].(2014-01-15)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/201401-663.点此复制
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