Increase in reactive nitrogen species production in chronic obstructive pulmonary disease airways
Increase in reactive nitrogen species production in chronic obstructive pulmonary disease airways
复制标题
DOI：
10.1164/ajrccm.162.2.9908132
复制
发表时间：
2000-08-01
影响因子：
24.7
通讯作者：
Shirato, K
中科院分区：
文献类型：
--
作者：
Ichinose, M;Sugiura, H;Shirato, K
一氧化氮（NO）与超氧阴离子反应以及过氧化物酶依赖性机制中形成的过亚硝酸盐、二氧化氮和其他活性氮物质（RNS）具有强效的炎症作用。因此，这些分子的数量可能会增加，并在炎症性气道疾病中发挥作用。在本研究中，我们使用诱导痰技术获得的气道炎症细胞中硝基酪氨酸和诱导型NO合酶（iNOS）的免疫染色定量RNS，并定量慢性阻塞性肺疾病（COPD）受试者、哮喘受试者和健康受试者（HS）的呼出气NO浓度，在COPD和哮喘受试者的气道炎症细胞中观察到的iNOS免疫反应性显著高于HS，尽管只有哮喘患者呼出的NO水平升高。炎症细胞在COPD受试者中表现出明显的硝基酪氨酸免疫反应性，在哮喘受试者中表现出较低程度的硝基酪氨酸免疫反应性，但在HS中没有。在COPD受试者中，FEV的百分比预测值与硝基酪氨酸形成量之间存在显著的负相关性，但在哮喘和HS受试者中没有。这些结果表明：（1）RNS可能参与COPD气道炎症和阻塞过程的病理生物学;（2）气道中产生的NO（可能通过iNOS）通过与超氧阴离子和/或过氧化物酶依赖性机制反应而消耗。
Peroxynitrite, nitrogen dioxide, and other reactive nitrogen species (RNS) that are formed in the reaction of nitric oxide (NO) with superoxide anion, and in peroxidase-dependent mechanisms, have a potent inflammatory action. These molecules may therefore increase in number and have a role in inflammatory airway diseases. In the present study, we quantified RNS using immunostaining of nitrotyrosine and inducible NO synthase (iNOS) in airway inflammatory cells obtained by the induced sputum technique, and also quantified the exhaled NO concentration in subjects with chronic obstructive pulmonary disease (COPD), subjects with asthma, and healthy subjects (HS), Immunoreactivity for iNOS observed in the airway inflammatory cells was significantly and similarly higher in subjects with COPD and asthma than in HS, although exhaled NO levels were increased only in subjects with asthma. Inflammatory cells showed obvious nitrotyrosine immunoreactivity in subjects with COPD and to a lesser extent in those with asthma, but not in HS, There was a significant negative correlation between the percent predicted values of FEV, and the amount of nitrotyrosine formation in subjects with COPD, but not in those with asthma and HS, These results suggest that: (1) RNS may be involved in the pathobiology of the airway inflammatory and obstructive process in COPD; and (2) NO produced in the airways, presumably via iNOS, is consumed by its reaction with superoxide anion and/or peroxidase-dependent mechanisms.