Aquatic Ecology and Toxicology Group, Department of Zoology, University of Heidelberg, Im Neuenheimer Feld 230, 69120, Heidelberg, Germany.
Environ Sci Pollut Res Int. 2010 Jul;17(6):1257-67. doi: 10.1007/s11356-010-0305-3. Epub 2010 Mar 1.
BACKGROUND, AIM, AND SCOPE: Lungs are permanently and simultaneously challenged by airborne microorganisms and airborne pollutants. Temporal increase of airborne particulate matter (APM), a potential carrier for extractable organic matter (EOM), degrades the situation of pulmonary patients. The Ah receptor (AhR) has been described as an important factor influencing the immunological challenge by viral infections. Molecular mechanisms underlying epidemiological observations are not well understood. Cytokine secretion (IL-6, IL-8, and TGF-beta) from human bronchial epithelial cells (Beas2B) was determined as an indicator for immune responses upon co-stimulation with an artificial analog of viral dsRNA [polyinosinic/polycytidylic acid, (PIC)] and EOM of Standard Reference Material 1649a (SRM). Since polycyclic aromatic hydrocarbons are major components of APM usually acting via the AhR, particular focus was on AhR involvement.
Cytokine secretion was demonstrated by enzyme-linked immunosorbent assay. To mimic the activation of organic matter during contact of particles with the human lung, Soxhlet extraction of SRM was performed. In some experiments, the AhR was blocked by alpha-naphthoflavone.
Microbial stimulation (PIC) induced Beas2B cytokine release, whereas isolated exposure to EOM of APM did not. Co-stimulation with EOM and PIC increased IL-8 secretion, whereas neither IL-6 nor TGF-beta was affected. Blocking of the AhR suppressed the release of IL-8.
Organic compounds adsorbed on airborne particulate matter influence the cytokine secretion of lung epithelial cells induced by pathogen-associated molecular patterns.
Further investigation of these observations is required to understand the molecular mechanisms underlying adverse health effects of APM reported in epidemiological studies.
背景、目的和范围:空气中的微生物和污染物会持续且同时对肺部造成挑战。空气中颗粒物(APM)的时间增加,APM 是可提取有机物(EOM)的潜在载体,使肺部患者的情况恶化。芳香烃受体(AhR)已被描述为影响病毒感染引起的免疫挑战的重要因素。但目前尚不清楚流行病学观察结果的分子机制。来自人支气管上皮细胞(Beas2B)的细胞因子(IL-6、IL-8 和 TGF-β)分泌被确定为免疫反应的指标,当与病毒双链 RNA [聚肌苷酸/聚胞苷酸,(PIC)]的人工类似物和标准参考物质 1649a(SRM)的 EOM 共刺激时。由于多环芳烃是 APM 的主要成分,通常通过 AhR 起作用,因此特别关注 AhR 的参与。
通过酶联免疫吸附试验证明细胞因子分泌。为了模拟颗粒物与人肺接触时有机物的激活,对 SRM 进行了索氏提取。在一些实验中,AhR 被α-萘黄酮阻断。
微生物刺激(PIC)诱导 Beas2B 细胞因子释放,而单独暴露于 APM 的 EOM 则不会。EOM 和 PIC 共刺激增加了 IL-8 的释放,而 IL-6 和 TGF-β均不受影响。AhR 阻断抑制了 IL-8 的释放。
吸附在空气中颗粒物上的有机化合物会影响与病原体相关的分子模式诱导的肺上皮细胞细胞因子的分泌。
需要进一步研究这些观察结果,以了解流行病学研究中报告的 APM 对健康的不利影响的分子机制。