Immunology Department, IIS-Fundación Jiménez-Díaz, Madrid, Spain.
Prostaglandins Other Lipid Mediat. 2011 Aug;95(1-4):11-8. doi: 10.1016/j.prostaglandins.2011.03.002. Epub 2011 Mar 30.
Non-asthmatic eosinophilic bronchitis (NAEB) is characterized by chronic cough and sputum eosinophilia without bronchial hyperresponsiveness. The aim of the present study is to determine whether increased levels of PGE(2) from NAEB sputum supernatants play a protective role in airway inflammation and muscular hyperplasia. Twenty-one patients with NAEB, 15 asthmatic patients, and 12 healthy subjects were studied. An up-regulated PGE(2) enzymatic pathway was observed in bronchial biopsies from patients with NAEB as compared with samples from asthmatic patients. Also, EP2 and EP4 receptor expression was increased in these samples. BSMC proliferation was inhibited to a greater extent in NAEB sputum supernatants than in those taken from asthmatic subjects and healthy controls. This inhibition was mostly due to PGE(2) levels, a fact which was confirmed by employing synthetic EP2 and EP4 agonist and antagonist receptors.These findings suggest that PGE(2) inhibits BSMC proliferation entailing a reduction of smooth muscle hyperplasia and thus protecting against the onset of airflow obstruction.
非哮喘性嗜酸性支气管炎（NAEB）的特征是慢性咳嗽和痰嗜酸性粒细胞增多，而无支气管高反应性。本研究旨在确定 NAEB 痰上清液中增加的 PGE（2）水平是否在气道炎症和肌肉增生中发挥保护作用。研究了 21 名 NAEB 患者、15 名哮喘患者和 12 名健康受试者。与哮喘患者的样本相比，在 NAEB 患者的支气管活检中观察到 PGE（2）酶途径上调。此外，这些样本中 EP2 和 EP4 受体表达增加。与哮喘患者和健康对照组的痰上清液相比，NAEB 痰上清液对 BSMC 增殖的抑制作用更大。这种抑制主要归因于 PGE（2）水平，这一事实通过使用合成的 EP2 和 EP4 激动剂和拮抗剂受体得到了证实。这些发现表明，PGE（2）抑制 BSMC 增殖，减少平滑肌增生，从而防止气流阻塞的发生。
