Tsoumakidou Maria, Tzanakis Nikolaos, Chrysofakis Georgios, Siafakas Nikolaos M
Department of Thoracic Medicine, University of Crete, Medical School, PO Box 1352, 71110 Heraklion, Crete, Greece.
Chest. 2005 Jun;127(6):1911-8. doi: 10.1378/chest.127.6.1911.
The aim of this study was to examine the relationship between airway inflammation, nitrosative stress, heme-oxygenase expression, and acute severe exacerbations of COPD.
We measured heme oxygenase (HO)-1, inducible nitric oxide (NO) synthase expression and nitrotyrosine formation, as well as eosinophilic cationic protein, myeloperoxidase (MPO), interleukin (IL-8), and granulocyte macrophage-colony stimulating factor levels in induced sputum samples from 12 COPD patients (mean +/- SD; FEV1 40 +/- 14% predicted) at the onset of an acute severe exacerbation of COPD requiring hospital admission and 16 weeks after remission.
We demonstrated increased percentages (p = 0.001) and absolute numbers (p = 0.028) of total nitrotyrosine positive (+ve) inflammatory cells (ie, polymorphonuclear cells and macrophages), increased percentages (p = 0.04) and absolute numbers (p = 0.05) of total HO-1 +ve inflammatory cells, and increased MPO (p = 0.005) and IL-8 levels (p = 0.028) during severe exacerbation compared with the stable state.
Our results support the hypothesis of an involvement of inflammatory and nitrosative stress in severe COPD exacerbations. Future therapeutic strategies may aim at regulating inflammation and NO synthesis during COPD exacerbations.
本研究旨在探讨气道炎症、亚硝化应激、血红素加氧酶表达与慢性阻塞性肺疾病（COPD）急性重度加重之间的关系。
我们测量了12例因COPD急性重度加重需住院治疗的患者（平均±标准差；预计第一秒用力呼气容积[FEV1]为40±14%）在急性重度加重发作时及缓解后16周诱导痰样本中的血红素加氧酶（HO）-1、诱导型一氧化氮（NO）合酶表达、硝基酪氨酸形成，以及嗜酸性阳离子蛋白、髓过氧化物酶（MPO）、白细胞介素（IL）-8和粒细胞巨噬细胞集落刺激因子水平。
我们发现，与稳定状态相比，重度加重期总硝基酪氨酸阳性（+ve）炎症细胞（即多形核细胞和巨噬细胞）的百分比（p = 0.001）和绝对数量（p = 0.028）增加，总HO-1 +ve炎症细胞的百分比（p = 0.04）和绝对数量（p = 0.05）增加，MPO（p = 0.005）和IL-8水平（p = 0.028）增加。
我们的结果支持炎症和亚硝化应激参与重度COPD加重的假说。未来的治疗策略可能旨在调节COPD加重期间的炎症和NO合成。
