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在居民区采集的 PM2.5 会引起小鼠的 Th1 型炎症反应和氧化应激。

PM 2.5 collected in a residential area induced Th1-type inflammatory responses with oxidative stress in mice.

机构信息

Environmental Health Risk Research Department, National Institute of Environmental Research, Kyungseo-dong, Seo-gu, Incheon 404-708, Republic of Korea.

出版信息

Environ Res. 2011 Apr;111(3):348-55. doi: 10.1016/j.envres.2010.11.001. Epub 2011 Jan 21.

DOI:10.1016/j.envres.2010.11.001
PMID:21256479
Abstract

Epidemiologists have tried to establish an association between human health and exposure to particulate matter (PM). In addition, many researchers have investigated the adverse effects of PM as a trigger of cardiovascular and pulmonary diseases. It is known that a number of environmental contaminants are attached to PM and the toxicity of PM may depend on the sources. We investigated the effects of PM collected in a residential area of Seoul on the immunotoxic responses including cytokine production in BAL fluid and in blood after a single intratracheal instillation in mice with the characterization of physico-chemical properties of PM 2.5 samples. As results, pro-inflammatory cytokines (IL-1, TNF-α, and IL-6), Th0-type cytokine (IL-2), and Th1-type cytokines (IL-12 and IFN-γ) were increased by a dose-dependent manner. Cell infiltration in the alveolar area and phagocytosis by macrophage was observed until day 28 after instillation. The expressions of oxidative stress-related genes (HSP 1a, HSP 8, and SOD) and tissue damage-related genes (MMP-15, -19, and Slpi) were time-dependently increased. PM 2.5 also induced an increase of T cell distribution in lymphocyte and decreased the CD4+/CD8+ ratio. Based on the results, we suggest that PM 2.5 collected in a residential area of Seoul may induce Th1 type-inflammatory responses with oxidative stress and trigger adverse effects in human health.

摘要

流行病学研究人员试图建立人类健康与暴露于颗粒物(PM)之间的关联。此外,许多研究人员已经研究了 PM 作为心血管和肺部疾病诱因的不良影响。众所周知,许多环境污染物附着在 PM 上,并且 PM 的毒性可能取决于来源。我们研究了在首尔居民区收集的 PM 对免疫毒性反应的影响,包括单次气管内滴注 PM2.5 样品后 BAL 液和血液中细胞因子的产生,并对 PM2.5 样品的理化特性进行了表征。结果表明,促炎细胞因子(IL-1、TNF-α 和 IL-6)、Th0 型细胞因子(IL-2)和 Th1 型细胞因子(IL-12 和 IFN-γ)呈剂量依赖性增加。滴注后 28 天,肺泡区细胞浸润和巨噬细胞吞噬作用增加。与氧化应激相关的基因(HSP 1a、HSP 8 和 SOD)和组织损伤相关基因(MMP-15、-19 和 Slpi)的表达呈时间依赖性增加。PM2.5 还诱导淋巴细胞中 T 细胞分布增加,CD4+/CD8+ 比值降低。基于这些结果,我们认为首尔居民区采集的 PM2.5 可能会引发 Th1 型炎症反应和氧化应激,并对人类健康产生不良影响。

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