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Cytokine expression in mice exposed to diesel exhaust particles by inhalation. Role of tumor necrosis factor

机译:通过吸入暴露于柴油机排气颗粒的小鼠中的细胞因子表达。肿瘤坏死因子的作用

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摘要

BackgroundParticulate air pollution has been associated with lung and cardiovascular disease, for which lung inflammation may be a driving mechanism. The pro-inflammatory cytokine, tumor necrosis factor (TNF) has been suggested to have a key-role in particle-induced inflammation.We studied the time course of gene expression of inflammatory markers in the lungs of wild type mice and Tnf-/- mice after exposure to diesel exhaust particles (DEPs). Mice were exposed to either a single or multiple doses of DEP by inhalation. We measured the mRNA level of the cytokines Tnf and interleukin-6 (Il-6) and the chemokines, monocyte chemoattractant protein (Mcp-1), macrophage inflammatory protein-2 (Mip-2) and keratinocyte derived chemokine (Kc) in the lung tissue at different time points after exposure.
机译:背景空气中的颗粒物污染与肺部疾病和心血管疾病有关,而肺部炎症可能是导致这种疾病的驱动机制。促炎细胞因子,肿瘤坏死因子(TNF)被认为在颗粒诱导的炎症中起关键作用。我们研究了野生型小鼠和Tnf-/-肺中炎症标志物基因表达的时程。暴露于柴油机尾气颗粒(DEP)后的小鼠。通过吸入使小鼠暴露于单剂量或多剂量的DEP。我们测量了细胞因子Tnf和白介素6(Il-6)和趋化因子,单核细胞趋化蛋白(Mcp-1),巨噬细胞炎性蛋白2(Mip-2)和角化细胞衍生趋化因子(Kc)的mRNA水平。暴露后不同时间点的肺组织。

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