大气细颗粒物致动脉粥样硬化小鼠肺脏炎性损伤

目的 探讨大气细颗粒物对动脉粥样硬化小鼠肺脏的炎性损伤及机制。方法 采集上海市区大气细颗粒物（PM_2.5），选用ApoE-/-小鼠（动脉粥样硬化模型）和C57BL/6小鼠（对照）各32只，进行气管滴注PM_2.5染毒，隔天滴注1次，共2次，根据染毒剂量的不同分为低、中、高剂量组；取小鼠肺泡灌洗液进行白介素6（IL-6）、IL-17、肿瘤坏死因子α（TNF-α）水平检测，细胞分类计数，取肺组织进行病理学观察。结果 与对照组比较，高剂量染毒组ApoE-/-小鼠肺泡灌洗液中IL-6、IL-17、TNF-α水平[（207.08±33.51）、（119.20±17.92）、（117.18±15.22）pg/mL]明显升高；与对照组比较，中、高剂量染毒组C57BL/6小鼠肺泡灌洗液中IL-6、IL-17、TNF-α水平升高；细胞分类计数结果显示，ApoE-/-小鼠肺泡灌洗液中中性粒细胞百分比、巨噬细胞绝对数随染毒剂量增加而增加，淋巴细胞百分比随染毒剂量升高而降低；肺脏组织病理切片显示，高剂量染毒组ApoE-/-小鼠和C57BL/6小鼠肺泡壁增厚显著，肺泡间隔增宽，部分区域可见肺实变表现，肺泡支气管旁可见多灶淋巴组织浸润。结论 与C57BL/6小鼠比较，大气细颗粒物急性暴露可引起ApoE-/-小鼠更为严重的肺脏炎症。

Effect of airborne fine particulate matter on atherosclerotic lung inflammatory injury in mice

Objective To explore the effect of airborne fine particulate matter on lung inflammatory injury and its mechanism in C57BL/6 mice with atherosclerosis.Methods Particulate matter less than 2.5 microns in aerodynamic diameter (PM_2.5) in ambient air were collected with glass fiber filters in a non-industry area of Shanghai,China.Eight-weeks old ApoE-/-mice were fed with high-fat diet for 8 weeks to establish an atherosclerosis model.Then the ApoE-/-mice and their littermates C57BL/6 mice were exposed to PM_2.5 by intratracheal instillation at the dosages of 0.0 (control),3.0,10.0,and 30.0 mg/kg bw,respectively.The treatments were conducted once a day in every other day for three days.Twenty-four hours after the last treatment,bronchoalveolar lavage fluid (BALF) samples of the mice were collected for the determinations of interleukin-6 (IL-6),interleukin-17 (IL-17),and tumor necrosis factor alpha,(TNF-α) and total and differential leukocyte count.Lung tissue samples were also collected for pathological examination.Results The contents of IL-6 (207.08±33.51 pg/mL),IL-17 (119.20±17.92 pg/mL),and TNF-α (117.18±15.22 pg/mL) in BALF of the ApoE-/-mice exposed to high dose PM_2.5 increased significantly compared to those of the mice of the control group; the contents of IL-6,IL-17,and TNF-α in BALF of the C57BL/6 mice exposed to moderate and high dose PM_2.5 increased compared to those of the mice of the control group.The percentage of neutrophils and absolute number of macrophage increased and the percentage of lymphocytes decreased in BALF of the ApoE-/-mice with the increment of PM_2.5 exposure dose.The thickening of alveolar wall,the widening of interval between alveoli,pulmonary consolidation,and multiple lymphocyte infiltration around bronchi were observed in the ApoE-/-and C57BL/6 mice exposed to high dose PM_2.5.Conclusion Acute exposure of fine particulate matter in ambient air could induce much more severe lung inflammatory injury in ApoE-/-mice than in C57BL/6 mice.