Pulmonary inflammation induced by low-dose particulate matter exposure in mice
Pulmonary inflammation induced by low-dose particulate matter exposure in mice
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DOI：
10.1152/ajplung.00232.2019
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发表时间：
2019-09-01
影响因子：
4.9
通讯作者：
Oliver, Brian Gregory George
中科院分区：
文献类型：
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作者：
Chan, Yik Lung;Wang, Baoming;Oliver, Brian Gregory George
空气污染是一个普遍存在的问题，包括气体和颗粒物（PM）。流行病学研究清楚地表明，暴露于PM与肺功能受损和肺部疾病（如慢性阻塞性肺病和哮喘）的发展有关。为了理解所涉及的机制，通常使用动物模型。然而，大多数这类模型代表了高水平的接触，并不能代表澳大利亚等污染较少国家的接触水平。因此，在这项研究中，我们的目的是确定低剂量的PM10暴露是否对肺部有任何不利影响。小鼠鼻内暴露于生理盐水或交通相关的PM10（1 μ g或5 μ g/天）3周。分析支气管肺泡灌洗（BAL）和肺组织。1 μ g的PM10对炎症和线粒体标志物没有显著影响。在5 μ g时，PM10暴露增加了BAL液中的淋巴细胞和巨噬细胞。PM10暴露后，NACHT、LRR和PYD结构域蛋白3（NLRP 3）和IL-1 β的产生增加。PM10（5 μ g）暴露降低了线粒体抗氧化剂超氧化锰（抗氧化防御系统）和线粒体融合标记（OPA-1），而增加了裂变标记（Drp-1）。自噬标志物轻链3微管相关蛋白（LC 3）-II和磷酸化AMPK减少，凋亡标志物（caspase 3）增加。未观察到重塑标志物的显著变化。总之，亚慢性低水平暴露于PM可能对肺部健康产生不利影响，在规划道路和住宅建筑时应考虑到这一点。
Air pollution is a ubiquitous problem and comprises gaseous and particulate matter (PM). Epidemiological studies have clearly shown that exposure to PM is associated with impaired lung function and the development of lung diseases, such as chronic obstructive pulmonary disease and asthma. To understand the mechanisms involved, animal models are often used. However, the majority of such models represent high levels of exposure and are not representative of the exposure levels in less polluted countries, such as Australia. Therefore, in this study, we aimed to determine whether low dose PM10 exposure has any detrimental effect on the lungs. Mice were intranasally exposed to saline or traffic-related PM10 (1 mu g or 5 mu g/day) for 3 wk. Bronchoalveolar lavage (BAL) and lung tissue were analyzed. PM10 at 1 mu g did not significantly affect inflammatory and mitochondrial markers. At 5 mu g, PM10 exposure increased lymphocytes and macrophages in BAL fluid. Increased NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and IL-1 beta production occurred following PM10 exposure. PM10 (5 mu g) exposure reduced mitochondrial antioxidant manganese superoxide (antioxidant defense system) and mitochondrial fusion marker (OPA-1), while it increased fission marker (Drp-1). Autophagy marker light-chain 3 microtubule-associated protein (LC3)-II and phosphorylated-AMPK were reduced, and apoptosis marker (caspase 3) was increased. No significant change of remodeling markers was observed. In conclusion, a subchronic low-level exposure to PM can have an adverse effect on lung health, which should be taken into consideration for the planning of roads and residential buildings.