Airborne Particulate Matter Induces Nonallergic Eosinophilic Sinonasal Inflammation in Mice
Airborne Particulate Matter Induces Nonallergic Eosinophilic Sinonasal Inflammation in Mice
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DOI：
10.1165/rcmb.2016-0351oc
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发表时间：
2017-07-01
影响因子：
6.4
通讯作者：
Biswal, Shyam
中科院分区：
文献类型：
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作者：
Ramanathan, Murugappan, Jr.;London, Nyall R., Jr.;Biswal, Shyam
暴露在空气中的颗粒物(PM)与呼吸道症状加重、心血管疾病风险增加和全因死亡有关。尽管PM对下肺气道的健康影响已被广泛研究，但关于慢性PM暴露对上鼻窦气道的影响却知之甚少。我们试图在活体内测试慢性空气PM暴露对上呼吸道系统的影响。小鼠吸入高浓度细颗粒物(2.5微米)，每天6小时，每周5天，共16周。空气中细颗粒物的平均浓度为60.92 mm/m(3)，低于全球一些主要城市的报告浓度。然后将小鼠处死，并与对照组小鼠相比，分析炎症和屏障破坏的证据。有证据表明，慢性空气颗粒物对活体鼻腔健康的破坏性影响，包括促炎细胞因子的释放，以及巨噬细胞和中性粒细胞炎性细胞的聚集。通过鼻道灌洗液中白蛋白的积聚以及包括Claudin-1和上皮钙粘附素在内的黏附分子表达的减少，观察到上皮屏障功能障碍的显著增加。嗜酸性炎症显著增加，包括IL-13、嗜酸性粒细胞聚集和嗜酸性粒细胞增多。总的来说，尽管这些研究主要是观察性的，但这些研究证明了长期暴露在空气中的PM对小鼠鼻腔气道屏障破坏和非过敏性嗜酸性炎症的破坏性影响。
Exposure to airborne particulate matter (PM) has been linked to aggravation of respiratory symptoms, increased risk of cardiovascular disease, and all-cause mortality. Although the health effects of PM on the lower pulmonary airway have been extensively studied, little is known regarding the impact of chronic PM exposure on the upper sinonasal airway. We sought to test the impact of chronic airborne PM exposure on the upper respiratory system in vivo. Mice were subjected, by inhalation, to concentrated fine (2.5 mu m) PM 6 h/d, 5 d/wk, for 16 weeks. Mean airborne fine PM concentration was 60.92 mm/m(3), a concentration of fine PM lower than that reported in some major global cities. Mice were then killed and analyzed for evidence of inflammation and barrier breakdown compared with control mice. Evidence of the destructive effects of chronic airborne PM on sinonasal health in vivo, including proinflammatory cytokine release, and macrophage and neutrophil inflammatory cell accumulation was observed. A significant increase in epithelial barrier dysfunction was observed, as assessed by serum albumin accumulation in nasal airway lavage fluid, as well as decreased expression of adhesion molecules, including claudin-1 and epithelial cadherin. A significant increase in eosinophilic inflammation, including increased IL-13, eotaxin-1, and eosinophil accumulation, was also observed. Collectively, although largely observational, these studies demonstrate the destructive effects of chronic airborne PM exposure on the sinonasal airway barrier disruption and nonallergic eosinophilic inflammation in mice.