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首页> 外文期刊>American Journal of Physiology >Chronic obstructive pulmonary disease and neutrophil infiltration: role of cigarette smoke and cyclooxygenase products.
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Chronic obstructive pulmonary disease and neutrophil infiltration: role of cigarette smoke and cyclooxygenase products.

机译：慢性阻塞性肺疾病和中性粒细胞浸润：香烟烟雾和环氧合酶产物的作用。

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Cigarette smoke is the main cause of chronic obstructive pulmonary disease (COPD), where it can contribute to the observed airway inflammation. PGE(2) is produced within human airways, and both pro- and anti-inflammatory activities have been reported. We quantitated PGE(2) concentrations in induced sputum supernatants from different groups of subjects and correlated the obtained values to neutrophil infiltration as well as to the expression of cyclooxygenase-2 (COX-2). Cigarette smoke extract (CSE) was used to evaluate the effect of smoking on COX-2 and PGE(2) receptor expression as well as on PGE(2) release in neutrophils and alveolar macrophages (AM) obtained from normal donors. The effects of PGE(2) and of PGE receptor agonists and antagonists were evaluated on the adhesion of neutrophil to a human bronchial epithelial cell line (16HBE). PGE(2) levels, COX-2 expression, and neutrophil infiltration were significantly higher in normal smokers and COPD smokers (P < 0.0001) compared with controls and COPD former smokers. Induced sputum supernatant caused neutrophil adhesion to 16HBE that was significantly reduced, in COPD smokers only, by PGE(2) immunoprecipitation. In vitro experiments confirmed that CSE increased PGE(2) release and COX-2 and PGE(2) receptor expression in neutrophils and AM; PGE(2) enhanced the adhesion of neutrophils to 16HBE, and a specific E-prostanoid 4 (EP(4)) receptor antagonist blunted its effect. These results suggest that CSE promote the induction of COX-2 and contributes to the proinflammatory effects of PGE(2) in the airways of COPD subjects.
机译：香烟烟雾是慢性阻塞性肺疾病（COPD）的主要原因，它可以导致观察到的气道炎症。 PGE（2）在人的呼吸道内产生，并且已经报道了促炎和消炎活性。我们量化了来自不同组受试者的痰液上清液中的PGE（2）浓度，并将获得的值与嗜中性粒细胞浸润以及环氧合酶-2（COX-2）的表达相关。香烟烟雾提取物（CSE）用于评估吸烟对从正常供体获得的嗜中性粒细胞和肺泡巨噬细胞（AM）中COX-2和PGE（2）受体表达以及PGE（2）释放的影响。评估了PGE（2）以及PGE受体激动剂和拮抗剂对嗜中性粒细胞与人支气管上皮细胞系（16HBE）粘附的影响。与对照组和以前的COPD吸烟者相比，正常吸烟者和COPD吸烟者的PGE（2）水平，COX-2表达和中性粒细胞浸润显着更高（P <0.0001）。诱导痰上清液导致中性粒细胞粘附于16HBE，仅在COPD吸烟者中通过PGE（2）免疫沉淀而显着降低。体外实验证实，CSE可增加嗜中性粒细胞和AM中PGE（2）的释放以及COX-2和PGE（2）受体的表达。 PGE（2）增强了嗜中性粒细胞对16HBE的粘附，而特定的E-前列腺素4（EP（4））受体拮抗剂减弱了其作用。这些结果表明，CSE促进了COX-2的诱导，并有助于COPD受试者气道中PGE（2）的促炎作用。

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