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In vivo immune activation of splenocytes following exposure to tar from Asian sand dust.
Journal of Toxicology and Environmental Health, Part A ( IF 2.6 ) Pub Date : 2020-08-20 , DOI: 10.1080/15287394.2020.1806160
Mengyue Shen 1 , Yuan Song 1, 2 , Takamichi Ichinose 3 , Kentaro Morita 1 , Duo Wang 1 , Keiichi Arashidani 1 , Yasuhiro Yoshida 1
Affiliation  

Air pollution, especially that initiated by particulate matter (PM), has been implicated as a risk factor for several inflammatory diseases. Previously, it was reported that PM enhances immune responses. PM includes the tar fraction that contains polycyclic aromatic hydrocarbons (PAHs), which produce adverse health effects in exposed individuals. However, the influence of the tar fraction (as a component of PM) on splenocytes is not fully understood. The aim of this study was to determine the effects of the tar fraction extracted from PM collected from the atmosphere in Fukuoka, Japan, on mouse splenocytes. ICR mice were administered tar (1 or 5 μg/mouse) intratracheally 4 times at 2-week intervals, and splenocytes from the tar-treated mice were extracted and examined. The parameters determined were proliferation, cytokine concentrations and transcription factors activation. Following tar treatment, splenocyte proliferation increased relative to controls. Concanavalin A (ConA)-induced interleukin (IL)-2 formation and ConA- or lipopolysaccharide (LPS)-induced interferon-γ production were elevated in splenocytes from tar-exposed mice. However, the production of tumor necrosis factor-α and IL-6 induced by LPS was not markedly changed following tar treatment. Further, nuclear factor of activated T cells, but not nuclear factor-κB, was enhanced in splenocytes of tar-exposed mice. Data indicate that tar-activated splenocytes and PM-bound PAHs might contribute to T cell activation in the spleen.



中文翻译:

暴露于亚洲沙尘中的焦油后,脾细胞的体内免疫激活。

空气污染,特别是由颗粒物(PM)引发的空气污染,被认为是几种炎症性疾病的危险因素。以前,有报道说PM可以增强免疫反应。PM包含含有多环芳烃(PAH)的焦油馏分,会对暴露的个体产生不利的健康影响。但是,尚不完全了解焦油级分(作为PM的成分)对脾细胞的影响。这项研究的目的是确定从日本福冈市大气中收集的PM中提取的焦油馏分对小鼠脾细胞的影响。ICR小鼠每2周间隔气管内施用tar(1或5μg/小鼠)4次,提取并检查来自tar治疗小鼠的脾细胞。确定的参数是增殖,细胞因子浓度和转录因子激活。焦油处理后,脾细胞增殖相对于对照组增加。焦油暴露小鼠脾细胞中伴刀豆球蛋白A(ConA)诱导的白介素(IL)-2的形成和ConA或脂多糖(LPS)诱导的干扰素-γ的产生增加。但是,焦油处理后,LPS诱导的肿瘤坏死因子-α和IL-6的产生没有明显改变。此外,在暴露于焦油的小鼠的脾细胞中,活化的T细胞的核因子而不是核因子-κB增强。数据表明焦油激活的脾细胞和结合PM的PAHs可能有助于脾脏T细胞的激活。焦油暴露小鼠脾细胞中伴刀豆球蛋白A(ConA)诱导的白介素(IL)-2的形成和ConA或脂多糖(LPS)诱导的干扰素-γ的产生增加。但是,焦油处理后,LPS诱导的肿瘤坏死因子-α和IL-6的产生没有明显改变。此外,在暴露于焦油的小鼠的脾细胞中,活化的T细胞的核因子而不是核因子-κB增强。数据表明焦油激活的脾细胞和结合PM的PAHs可能有助于脾脏T细胞的激活。焦油暴露小鼠脾细胞中伴刀豆球蛋白A(ConA)诱导的白介素(IL)-2的形成和ConA或脂多糖(LPS)诱导的干扰素-γ的产生增加。但是,焦油处理后,LPS诱导的肿瘤坏死因子-α和IL-6的产生没有明显改变。此外,在暴露于焦油的小鼠的脾细胞中,活化的T细胞的核因子而不是核因子-κB增强。数据表明焦油激活的脾细胞和结合PM的PAHs可能有助于脾脏T细胞的激活。暴露于焦油的小鼠脾细胞中的α-β-内化酶增强。数据表明焦油激活的脾细胞和结合PM的PAHs可能有助于脾脏T细胞的激活。暴露于焦油的小鼠脾细胞中的α-β-内化酶增强。数据表明,焦油激活的脾细胞和结合PM的PAHs可能有助于脾脏T细胞的激活。

更新日期:2020-09-08
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