Hollins Fay, Sutcliffe Amanda, Gomez Edith, Berair Rachid, Russell Richard, Szyndralewiez Cédric, Saunders Ruth, Brightling Christopher
Institute for Lung Health, Department of Infection, Immunity & Inflammation, Glenfield Hospital, University of Leicester, Leicester, LE3 9QP, UK.
Genkyotex, Geneva, Switzerland.
Respir Res. 2016 Jul 19;17(1):84. doi: 10.1186/s12931-016-0403-y.
The burden of oxidative stress is increased in chronic obstructive pulmonary disease (COPD). However, whether the intra-cellular mechanisms controlling the oxidant/anti-oxidant balance in structural airway cells such as airway smooth muscle in COPD is altered is unclear. We sought to determine whether the expression of the NADPH oxidase (NOX)-4 is increased in airway smooth muscle in COPD both in vivo and primary cells in vitro and its role in hydrogen peroxide-induced reactive oxygen species generation. We found that in vivo NOX4 expression was up-regulated in the airway smooth muscle bundle in COPD (n = 9) and healthy controls with >20 pack year history (n = 4) compared to control subjects without a significant smoking history (n = 6). In vitro NOX4 expression was increased in airway smooth muscle cells from subjects with COPD (n = 5) compared to asthma (n = 7) and upregulated following TNF-α stimulation. Hydrogen peroxide-induced reactive oxygen species generation by airway smooth muscle cells in COPD (n = 5) was comparable to healthy controls (n = 9) but lower than asthma (n = 5); and was markedly attenuated by NOX4 inhibition. Our findings demonstrate that NOX4 expression is increased in vivo and in vitro in COPD and although we did not observe an intrinsic increase in oxidant-induced reactive oxygen species generation in COPD, it was reduced markedly by NOX4 inhibition supporting a potential therapeutic role for NOX4 in COPD.
慢性阻塞性肺疾病(COPD)中氧化应激负担增加。然而,尚不清楚COPD中诸如气道平滑肌等气道结构细胞内控制氧化剂/抗氧化剂平衡的机制是否发生改变。我们试图确定NADPH氧化酶(NOX)-4在COPD患者体内及原代细胞体外气道平滑肌中的表达是否增加,以及其在过氧化氢诱导的活性氧生成中的作用。我们发现,与无显著吸烟史的对照受试者(n = 6)相比,COPD患者(n = 9)及有>20包年吸烟史的健康对照者(n = 4)体内气道平滑肌束中的NOX4表达上调。在体外,与哮喘患者(n = 7)相比,COPD患者(n = 5)气道平滑肌细胞中的NOX4表达增加,且在肿瘤坏死因子-α刺激后上调。COPD患者(n = 5)气道平滑肌细胞由过氧化氢诱导的活性氧生成与健康对照者(n = 9)相当,但低于哮喘患者(n = 5);并且通过抑制NOX4可使其显著减弱。我们的研究结果表明,COPD患者体内及体外的NOX4表达均增加,尽管我们未观察到COPD患者中氧化剂诱导的活性氧生成有内在增加,但通过抑制NOX4可使其显著降低,这支持了NOX4在COPD中具有潜在治疗作用的观点。