Abstract: 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.