Lung inflammation caused by inhaled toxicants: a review.
Lung inflammation caused by inhaled toxicants: a review.
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DOI：
10.2147/copd.s106009
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发表时间：
2016
影响因子：
2.8
通讯作者：
Wood LJ
中科院分区：
文献类型：
--
作者：
Wong J;Magun BE;Wood LJ
肺部暴露于来自环境中不同来源的空气传播的有毒物质可能导致急性和慢性肺部甚至全身炎症。香烟烟雾是慢性阻塞性肺病的主要原因，尽管不发达国家城市地区的木材烟雾现在被认为是呼吸道疾病的主要原因。来自真菌孢子的真菌毒素会造成呼吸道疾病的职业风险，也会对居住在潮湿建筑物中的人造成健康危害。石棉和二氧化硅（来自建筑材料）的微小空气微粒和重金属（来自油漆）是室内空气污染的额外来源，有助于呼吸系统疾病，已知会导致实验动物的呼吸系统疾病。气雾形式的蓖麻毒素是一种潜在的生物武器，毒性极强，但相对容易生产。虽然上述制剂属于不同类别的有毒化学品，但它们的致病性是相似的。它们诱导巨噬细胞的募集和活化、促分裂原活化蛋白激酶的活化、蛋白质合成的抑制和白细胞介素-1 β的产生。靶向巨噬细胞（使用纳米颗粒）或白细胞介素-1 β的产生（使用蛋白激酶抑制剂，NOD样受体蛋白-3或P2 X7）可能用于治疗这些类型的肺部炎症，而不会影响对细菌感染的天然免疫反应。
Exposure of the lungs to airborne toxicants from different sources in the environment may lead to acute and chronic pulmonary or even systemic inflammation. Cigarette smoke is the leading cause of chronic obstructive pulmonary disease, although wood smoke in urban areas of underdeveloped countries is now recognized as a leading cause of respiratory disease. Mycotoxins from fungal spores pose an occupational risk for respiratory illness and also present a health hazard to those living in damp buildings. Microscopic airborne particulates of asbestos and silica (from building materials) and those of heavy metals (from paint) are additional sources of indoor air pollution that contributes to respiratory illness and is known to cause respiratory illness in experimental animals. Ricin in aerosolized form is a potential bioweapon that is extremely toxic yet relatively easy to produce. Although the aforementioned agents belong to different classes of toxic chemicals, their pathogenicity is similar. They induce the recruitment and activation of macrophages, activation of mitogen-activated protein kinases, inhibition of protein synthesis, and production of interleukin-1 beta. Targeting either macrophages (using nanoparticles) or the production of interleukin-1 beta (using inhibitors against protein kinases, NOD-like receptor protein-3, or P2X7) may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections.