The role of particulate pollutants in pulmonary inflammation and asthma: evidence for the involvement of organic chemicals and oxidative stress.
The role of particulate pollutants in pulmonary inflammation and asthma: evidence for the involvement of organic chemicals and oxidative stress.
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DOI：
10.1097/00063198-200101000-00004
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发表时间：
2001-01-01
影响因子：
3.3
通讯作者：
Li, N
中科院分区：
文献类型：
--
作者：
Nel, A E;Diaz-Sanchez, D;Li, N
我们回顾了文献表明，环境颗粒物的不良健康影响涉及氧化应激和炎症的产生，以及颗粒相关化学物质的免疫调节作用。我们讨论的证据表明，柴油机排气颗粒有机提取物诱导活性氧在巨噬细胞和支气管上皮细胞，两个关键的细胞类型的颗粒物在肺中的目标。活性氧通过激活蛋白-1和核因子-κ B信号通路激活参与过敏性炎症的细胞因子和趋化因子的启动子，这可能解释过敏性炎症的加重。有机柴油机排气颗粒化学物质还通过线粒体途径诱导支气管上皮细胞凋亡和坏死。这可能是哮喘中上皮脱落和支气管高反应性的原因。
We review the literature indicating that the adverse health effects of ambient particulate matter involve the generation of oxidative stress and inflammation, as well as immunomodulating effects by particle-associated chemicals. We discuss evidence that diesel exhaust particle organic extracts induce reactive oxygen species in macrophages and bronchial epithelial cells, two key cell types targeted by particulate matter in the lung. Reactive oxygen species activate the promoters of cytokines and chemokines involved in allergic inflammation through activator protein-1 and nuclear factor- kappaB signaling pathways, which may explain exacerbation of allergic inflammation. Organic diesel exhaust particle chemicals also induce apoptosis and necrosis in bronchial epithelial cells via a mitochondrial pathway. This may be responsible for epithelial shedding and bronchial hyperreactivity in asthma.