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目的:探讨空气颗粒物(PM)及香烟烟雾提取物(CSE)对人肺泡上皮细胞(A549细胞)和单核细胞(THP-1细胞)源性巨噬细胞功能的影响。方法:采用不同浓度的PM与CSE单独或叠加体外刺激A549细胞和THP-1细胞，应用CCK-8法检测细胞增殖，流式细胞术检测细胞凋亡，酶联免疫吸附试验检测炎症因子表达，实时聚合酶链式反应检测巨噬细胞极化标志物，免疫蛋白质印迹法检测紧密连接蛋白ZO-1、occludin、claudin的表达。结果:与空白对照组比较，0.5% CSE、50 mg/LPM单独刺激即可抑制A549细胞增殖；二者叠加刺激后，较CSE单独刺激组能够进一步抑制该细胞增殖活性，促进细胞凋亡；同时，在CSE存在时，PM可进一步促进A549细胞和THP-1细胞产生的炎症因子白细胞介素6及白细胞介素1β。PM单独或与CSE叠加均可降低A549细胞表达occludin。实时聚合酶链式反应结果显示，CSE与PM叠加进一步促进THP-1细胞表达CD80 mRNA。结论:PM能够进一步加重CSE暴露所导致的气道上皮抑制增殖、促进凋亡、炎症及巨噬细胞向M1型极化。“,”Objective:To investigate the effects of particulate matter(PM) and cigarette-smoke extract (CSE) on the function of human airway epithelial cells (A549) and monocyte (THP-1)-derived macrophages.Methods:In vitro A549 cells and THP-1 cells were exposed to different concentrations of PM and CSE, either alone or in combination.CCK-8 kit, flow cytometry and enzyme linked immunosorbent assay were employed to measure cell proliferation, apoptosis and production of inflammatory factors in these cells, respectively.Furthermore, real-time polymerase chain reaction and Western blot were used to measure mRNA encoding macrophage polarization markers and epithelial tight junction proteins (ZO-1, occludin and claudin).Results:Compared with the controls, CSE (0.5%) and PM (50 mg/L) alone inhibited the proliferation of A549 cells, which was further attenuated by the presence of CSE and PM together.Co-stimulation with CSE and PM was able to enhance inhibition of cell proliferation, apoptosis, and production of inflammatory cytokines interleukin-6 and interleukin-1β in these cells.PM alone or combination of PM and CSE could reduce the expression of occludin in A549 cells.Real-time polymerase chain reaction result showed that the combination of CSE and PM further promoted CD80 mRNA expression in THP-1 cells.Conclusions:PM can further aggravate inhibition of airway epithelial proliferation, apoptosis, inflammation and induce polarization of macrophages to M1 types.