Castañeda Alejandro R, Bein Keith J, Smiley-Jewell Suzette, Pinkerton Kent E
a Center for Health and the Environment, University of California , Davis , California , USA.
b Air Quality Research Center, University of California , Davis , California , USA.
J Toxicol Environ Health A. 2017;80(4):197-207. doi: 10.1080/15287394.2016.1222920. Epub 2017 May 11.
Ambient particulate matter (PM), a component of air pollution, exacerbates airway inflammation and hyperreactivity in asthmatic patients. Studies showed that PM possesses adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanism (or mechanisms) by which PM enhances the allergic response remains to be determined. The aim of this study was to assess how exposure to fine PM collected from Sacramento, CA, shapes the allergic airway immune response in BALB/c mice undergoing sensitization and challenge with ovalbumin (OVA). Eight-week-old BALB/c male mice were sensitized/challenged with phosphate-buffered saline (PBS/PBS; n = 6), PM/PBS (n = 6), OVA/OVA (n = 6), or OVA + PM/OVA (n = 6). Lung tissue, bronchoalveolar lavage fluid (BALF), and plasma were analyzed for cellular inflammation, cytokines, immunoglobulin E, and heme oxygenase-1 (HO-1) expression. Mice in the OVA + PM/OVA group displayed significantly increased airway inflammation compared to OVA/OVA animals. Total cells, macrophages, and eosinophils recovered in BALF were significantly elevated in the OVA + PM/OVA compared to OVA/OVA group. Histopathological grading indicated that OVA + PM/OVA treatment induced significant inflammation compared to OVA/OVA. Both immunoglobulin (Ig) E and tumor necrosis factor (TNF) α levels were significantly increased in OVA/OVA and OVA + PM /OVA groups compared to PBS/PBS control. The number of HO-1 positive alveolar macrophages was significantly elevated in lungs of mice treated with OVA + PM /OVA compared to OVA/OVA. Our findings suggest that fine PM enhances allergic inflammatory response in pulmonary tissue through mechanisms involving increased oxidative stress.
环境颗粒物(PM)是空气污染的一个组成部分,会加剧哮喘患者的气道炎症和高反应性。研究表明,PM具有类似佐剂的特性,可增强过敏性炎症反应;然而,PM增强过敏反应的机制仍有待确定。本研究的目的是评估暴露于从加利福尼亚州萨克拉门托采集的细颗粒物PM如何影响用卵清蛋白(OVA)致敏和激发的BALB/c小鼠的过敏性气道免疫反应。8周龄的BALB/c雄性小鼠分别用磷酸盐缓冲盐水(PBS/PBS;n = 6)、PM/PBS(n = 6)、OVA/OVA(n = 6)或OVA + PM/OVA(n = 6)进行致敏/激发。对肺组织、支气管肺泡灌洗液(BALF)和血浆进行细胞炎症、细胞因子、免疫球蛋白E和血红素加氧酶-1(HO-1)表达分析。与OVA/OVA组动物相比,OVA + PM/OVA组小鼠的气道炎症明显增加。与OVA/OVA组相比,OVA + PM/OVA组BALF中回收的总细胞、巨噬细胞和嗜酸性粒细胞显著升高。组织病理学分级表明,与OVA/OVA组相比,OVA + PM/OVA处理诱导了显著的炎症。与PBS/PBS对照组相比,OVA/OVA组和OVA + PM /OVA组的免疫球蛋白(Ig)E和肿瘤坏死因子(TNF)α水平均显著升高。与OVA/OVA组相比,用OVA + PM /OVA处理的小鼠肺中HO-1阳性肺泡巨噬细胞的数量显著升高。我们的研究结果表明,细颗粒物PM通过涉及氧化应激增加的机制增强肺组织中的过敏性炎症反应。