氧化应激和巨噬细胞：哮喘和COPD急性加重的驱动力？
2018/12/17
摘要
氧化应激是阻塞性气道疾病如哮喘和慢性阻塞性肺病（COPD）的共同特征。肺巨噬细胞是产生氧化剂的关键先天免疫细胞，在这些疾病中表现出极化模式异常和吞噬反应缺陷。这些特征是否以某种方式相互关联，以及它们是否在哮喘和COPD急性加重的发生和严重程度中发挥作用，目前仍知之甚少。了解氧化应激、巨噬细胞及其相互作用对于充分了解肺部疾病的急性恶化可能是有重要价值的。因此，该综述强调了关于氧化应激和巨噬细胞在哮喘和COPD急性加重中的作用的现有技术。文章表明，氧化应激可以减弱巨噬细胞功能，从而可能导致其对急性加重触发因素反应性的损伤，并可能导致气道中炎症的蔓延。
Oxidative stress and macrophages: driving forces behind exacerbations of asthma and COPD?
de Groot LES, van der Veen TA, Martinez FO, Hamann J, Lutter R, Melgert BN.
Abstract
Oxidative stress is a common feature of obstructive airway diseases like asthma and chronic obstructive pulmonary disease (COPD). Lung macrophages are key innate immune cells that can generate oxidants and are known to display aberrant polarization patterns and defective phagocytic responses in these diseases. Whether these characteristics are linked in one way or another and whether they contribute to the onset and severity of exacerbations in asthma and COPD remains poorly understood. Insight into oxidative stress, macrophages and their interactions may be important in fully understanding acute worsening of lung disease. This review therefore highlights the current state of the art regarding the role of oxidative stress and macrophages in exacerbations of asthma and COPD. It shows that oxidative stress can attenuate macrophage function, which may result in impaired responses towards exacerbating triggers and may contribute to exaggerated inflammation in the airways.
氧化应激是阻塞性气道疾病如哮喘和慢性阻塞性肺病（COPD）的共同特征。肺巨噬细胞是产生氧化剂的关键先天免疫细胞，在这些疾病中表现出极化模式异常和吞噬反应缺陷。这些特征是否以某种方式相互关联，以及它们是否在哮喘和COPD急性加重的发生和严重程度中发挥作用，目前仍知之甚少。了解氧化应激、巨噬细胞及其相互作用对于充分了解肺部疾病的急性恶化可能是有重要价值的。因此，该综述强调了关于氧化应激和巨噬细胞在哮喘和COPD急性加重中的作用的现有技术。文章表明，氧化应激可以减弱巨噬细胞功能，从而可能导致其对急性加重触发因素反应性的损伤，并可能导致气道中炎症的蔓延。
(中日友好医院呼吸与危重症医学科 顾宪民 摘译 林江涛 审校)
(Am J Physiol Lung Cell Mol Physiol. 2018 Dec 6. doi:0.1152/ajplung.00456.2018.)
(Am J Physiol Lung Cell Mol Physiol. 2018 Dec 6. doi:0.1152/ajplung.00456.2018.)
Oxidative stress and macrophages: driving forces behind exacerbations of asthma and COPD?
de Groot LES, van der Veen TA, Martinez FO, Hamann J, Lutter R, Melgert BN.
Abstract
Oxidative stress is a common feature of obstructive airway diseases like asthma and chronic obstructive pulmonary disease (COPD). Lung macrophages are key innate immune cells that can generate oxidants and are known to display aberrant polarization patterns and defective phagocytic responses in these diseases. Whether these characteristics are linked in one way or another and whether they contribute to the onset and severity of exacerbations in asthma and COPD remains poorly understood. Insight into oxidative stress, macrophages and their interactions may be important in fully understanding acute worsening of lung disease. This review therefore highlights the current state of the art regarding the role of oxidative stress and macrophages in exacerbations of asthma and COPD. It shows that oxidative stress can attenuate macrophage function, which may result in impaired responses towards exacerbating triggers and may contribute to exaggerated inflammation in the airways.
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