The Effects of Ambient Particulate Matter on Human Alveolar Macrophage Oxidative and Inflammatory Responses
The Effects of Ambient Particulate Matter on Human Alveolar Macrophage Oxidative and Inflammatory Responses
复制标题
DOI：
10.1080/15287390903248901
复制
发表时间：
2010-01-01
影响因子：
2.6
通讯作者：
Madden, M. C.
中科院分区：
文献类型：
--
作者：
Sawyer, K.;Mundandhara, S.;Madden, M. C.
流行病学和职业性研究表明，环境颗粒物(PM)和柴油废气颗粒物(DEP)对人类心肺健康具有有害影响，包括加重既往存在的肺部疾病和发展呼吸道感染。环境PM对肺细胞反应性的影响尚不清楚。2001-2002年秋末(11月)和夏初(6月)在北卡罗来纳州教堂山收集的人肺泡巨噬细胞(AM)暴露于SRM 1649(华盛顿特区，城市粉尘；UD)、SRM 2975(叉车柴油废气颗粒物；DEP)和细或粗环境PM。在PM暴露后，AM与脂多糖(LPS)、佛波酯(PMA)或钙离子载体A23817孵育6或24小时。UD和DEP显著抑制PM暴露后24小时的[图像遗漏]释放。UD暴露可显著抑制10g/mlLPS诱导的肿瘤坏死因子(TNF)-α、白介素6(IL-6)和IL-8的释放。DEP仅显著抑制肿瘤坏死因子和白介素6的释放。受抑制的细胞因子释放也可能是由于细胞细胞因子产生减少所致。数据表明，细胞因子释放的减少不是由于苯并[a]芘(BaP)的存在而产生的，苯并不是一种多环芳烃。比较内毒素、PMA和A23817对肿瘤坏死因子释放的影响，发现UD的抑制作用是内毒素依赖性的，而DEP的抑制作用可能跨多个机制发挥作用。11月和6月，教堂山PM暴露在脂多糖暴露之前刺激了TNF-和IL-8的释放。细、粗11月PM暴露可显著抑制LPS刺激后6h的TNF释放，但对LPS刺激后24 h的IL-8释放有明显的刺激作用。6月细粒和粗粒PM可抑制脂多糖暴露后IL-8的释放。数据表明，在细菌暴露前后，PM成分的季节性影响会影响AM的炎症反应。总体而言，PM暴露后AM对内毒素的免疫反应延迟或被抑制，表明暴露于周围PM可能会增加肺部对呼吸道感染的易感性。
Epidemiologic and occupational studies demonstrated that ambient particulate matter (PM) and diesel exhaust particles (DEP) exert deleterious effects on human cardiopulmonary health, including exacerbation of pre-existing lung disease and development of respiratory infections. The effects of ambient PM on lung cell responsiveness are poorly defined. Human alveolar macrophages (AM) were exposed to SRM 1649 (Washington, DC, urban dust; UD), SRM 2975 (forklift diesel exhaust particles; DEP), and fine or coarse ambient PM collected in Chapel Hill, NC, during the late fall (November) and early summer (June) of 2001-2002. AM were subsequently incubated with lipopolysaccharide (LPS), phorbol myristate acetate (PMA), or calcium ionophore A23817 for 6 or 24 h after PM exposure. UD and DEP markedly suppressed [image omitted] release 24 h post-PM exposure. UD exposure significantly inhibited tumor necrosis factor (TNF)-, interleukin (IL)-6, and IL-8 release after exposure to 10 g/ml LPS. DEP significantly suppressed only TNF- and IL-6 release. Suppressed cytokine release may also be produced by reduced cellular cytokine production. Data suggested that decreased cytokine release is not produced by the presence of benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon. Comparison of TNF- release after LPS, PMA, or A23817 revealed that suppressive effects of UD are LPS dependent, whereas inhibitory effects of DEP may work across multiple mechanistic pathways. November and June Chapel Hill PM exposure stimulated TNF- and IL-8 release before LPS exposure. Fine and coarse November PM exposure markedly suppressed TNF- release 6 h after LPS stimulation, but appeared to exert a stimulatory effect on IL-8 release 24 h after LPS exposure. June fine and coarse PM suppressed IL-8 release after LPS exposure. Data suggest that seasonal influences on PM composition affect AM inflammatory response before and after bacterial exposure. Overall, delayed or inhibited AM immune responses to LPS after PM exposure suggest human exposure to ambient PM may enhance pulmonary susceptibility to respiratory infections.