Surface components of airborne particulate matter induce macrophage apoptosis through scavenger receptors
Surface components of airborne particulate matter induce macrophage apoptosis through scavenger receptors
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DOI：
10.1006/taap.2002.9493
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发表时间：
2002-10-15
影响因子：
3.8
通讯作者：
Holian, A
中科院分区：
文献类型：
--
作者：
Obot, CJ;Morandi, MT;Holian, A
流行病学研究表明，城市地区的死亡率、哮喘发病率和其他呼吸系统疾病与空气中细颗粒物（PM）浓度的增加有关。然而，无论是PM的生物活性成分还是所报道的健康影响的生物学机制都没有得到阐明。许多研究已经暗示可溶性金属、强酸部分和/或PM的其他组分作为可能的生物活性介质。肺泡巨噬细胞（AM）凋亡，介导的清道夫受体（SR），可能是重要的炎症颗粒的反应。因此，本研究探讨了PM的有机和金属成分通过与SR相互作用诱导细胞凋亡的假设。从Balb/c小鼠新鲜分离的AM与未经处理或用Milli-Q水，丙酮或环己烷提取的PM 1648样品孵育，酸消化，或在100或500 degreesC加热。通过台盼蓝拒染法评估细胞活力，通过细胞形态学检查和细胞死亡ELISA证明细胞凋亡。未处理的PM诱导AM坏死和凋亡。有机提取、酸消化或高温处理PM可改变颗粒表面组成，细胞凋亡减少。未处理、丙酮提取和高热处理的PM诱导的细胞凋亡可被聚肌胞或2148抗体阻断。这些结果表明，PM诱导的细胞凋亡是由A类I/II型SR介导的。改变PM的表面特性干扰SR的识别，导致AM的凋亡减少。因此，通过去除一种或多种PM组分（如本研究中进行的各种处理）来改变表面化学性质足以改变PM生物活性。这些结果也可能有助于解释为什么来自许多不同来源的PM，其组成不同，都具有生物活性，因为重要的是整体基质，而不仅仅是一个组分。(C)2002 Elsevier Science（美国）。
Epidemiology studies have linked mortality, increased asthma morbidity, and other respiratory disorders in urban areas to increases in fine airborne particulate matter (PM) concentrations. However, neither the bioactive components of PM nor the biological mechanisms of the reported health effects have been elucidated. A number of studies have implicated soluble metals, the strong acid fraction, and/or other components of PM as possible bioactive mediators. Alveolar macrophage (AM) apoptosis, mediated through scavenger receptors (SR), may be important in the response to inflammatory particles. Therefore, this study explores the hypothesis that organic and metallic components of PM induce apoptosis by interacting with SR. Freshly isolated AM from Balb/c mice were incubated with PM 1648 samples untreated or extracted with Milli-Q water, acetone, or cyclohexane, acid digested, or heated at 100 or 500degreesC. Cell viability was assessed by trypan blue exclusion and apoptosis was demonstrated by examination of cell morphology and cell death ELISA. Untreated PM induced necrosis and apoptosis in AM. Treatment of PM by organic extraction, acid digestion, or high heat modified the particle surface composition and apoptosis was decreased. Apoptosis induced by untreated, acetone extracted, and high heat-treated PM was blocked by polyinosinic acid or 2148 antibody. These results demonstrate that PM-induced apoptosis is mediated by Class A Type I/II SR. Altering the surface characteristics of PM interferes with recognition by SR, resulting in decreased apoptosis of AM. Therefore, altering the surface chemistry by removal of one or more PM components, such as the various treatments conducted in this study, is sufficient to alter PM bioactivity. These results may also help explain why PM from many different sources, with differences in composition, are all bioactive, since it is the overall matrix that is important, not just one component. (C) 2002 Elsevier Science (USA).