Particulate matter induces cytokine expression in human bronchial epithelial cells
Particulate matter induces cytokine expression in human bronchial epithelial cells
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DOI：
10.1165/ajrcmb.25.3.4445
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发表时间：
2001-09-01
影响因子：
6.4
通讯作者：
Van Eeden, SF
中科院分区：
文献类型：
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作者：
Fujii, T;Hayashi, S;Van Eeden, SF
本研究旨在确定暴露于环境空气污染颗粒（EHC-93）的原代人支气管上皮细胞（HBEC）产生的细胞因子。使用核糖核酸酶保护测定法测量细胞因子信使 RNA (mRNA)，并通过酶联免疫吸附测定法测量细胞因子蛋白的产生。从手术肺中新鲜分离原代HBEC，培养至汇合，并暴露于10至500μg/ml直径小于10μm的环境颗粒物（PM10）悬浮液中2、8和24小时。暴露于 PM10 后，白血病抑制因子 (LIF)、粒细胞巨噬细胞集落刺激因子 (GM-CSF)、白介素 (IL)-1 α 和 IL-8 的 mRNA 水平增加，且这种增加在 100 (P < 0.05) 和 500 (P < 0.05) mug/ml PM10 暴露之间呈剂量依赖性。 24小时收集的上清液中测得的LIP、GM-CSF、IL-1β和IL-8蛋白的浓度以剂量依赖性方式增加，并且显着高于对照未暴露细胞中的浓度。与对照值相比，PM10 可溶性部分 (100 μg/ml) 不会增加这些细胞因子 mRNA 水平，并且与暴露于 100 μg/ml PM10 的 HBEC 相比显着降低（LIF、IL-8 和 IL-1 beta；P < 0.05），GM-CSF mRNA 除外（P = 不显着）。我们的结论是，暴露于环境 PM10 的初级 HBEC 会产生促炎介质，促进局部和全身炎症反应，并且我们推测这些介质可能在与颗粒空气污染相关的心肺疾病的发病机制中发挥作用。
The present study was designed to determine cytokines produced by primary human bronchial epithelial cells (HBECs) exposed to ambient air pollution particles (EHC-93). Cytokine messenger RNA (mRNA) was measured using a ribonuclease protection assay and cytokine protein production by enzyme-linked immunosorbent assay. Primary HBECs were freshly isolated from operated lung, cultured to confluence, and exposed to 10 to 500 mug/ml of a suspension of ambient particulate matter with a diameter of less than 10 mum (PM10) for 2, 8, and 24 h. The mRNA levels of leukemia inhibitory factor (LIF), granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1 alpha, and IL-8 were increased after exposure to PM10, and this increase was dose-dependent between 100 (P < 0.05) and 500 (P < 0.05) mug/ml of PM10 exposure. The concentrations of LIP, GM-CSF, IL-1 beta, and IL-8 protein measured in the supernatant collected at 24 h increased in a dose-dependent manner and were significantly higher than those in the control nonexposed cells. The soluble fraction of the PM10 (100 mug/ml) did not increase these cytokine mRNA levels compared with control values and were significantly lower compared with HBECs exposed to 100 mug/ml of PM10 (LIF, IL-8, and IL-1 beta; P < 0.05), except for GM-CSF mRNA (P = not significant). We conclude that primary HBECs exposed to ambient PM10 produce proinflammatory mediators that contribute to the local and systemic inflammatory response, and we speculate that these mediators may have a role in the pathogenesis of cardiopulmonary disease associated with particulate air pollution.