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首页> 外文期刊>Chemosphere >Fine particulate matter from pig house induced immune response by activating TLR4/MAPK/NF-κB pathway and NLRP3 inflammasome in alveolar macrophages
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Fine particulate matter from pig house induced immune response by activating TLR4/MAPK/NF-κB pathway and NLRP3 inflammasome in alveolar macrophages

机译:猪房细颗粒物通过激活肺泡巨噬细胞中的TLR4 / MAPK /NF-κB途径和NLRP3炎性体诱导免疫反应

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摘要

Fine particulate matter (PM2.5) from livestock houses is harmful not only to the health and welfare of animals but also to the farmers working inside. As an important pollution source in the atmosphere environment, PM2.5 can threaten public health. PM2.5 collected from nursery pig house was studied. It included particulates of various morphologies, and the concentration of endotoxin was as high as to 681.80 EU/mg. To investigate the ability of PM2.5 from the nursery pig house to induce an immune response, porcine alveolar macrophages 3D4/21 cells were studied. The results showed that PM2.5 can induce cell death, ROS production and inflammatory cytokines release (IL-1 beta, IL-18, TNF-alpha and COX-2) by activating TLR4/MyD88 pathway and NLRP3 inflammasome. Furthermore, the downstream signaling pathways of TLR4/MyD88, MAPK and NF-kappa B, participated in NLRP3 inflammasome activation. To further study the role of endotoxin present in PM2.5 and the oxidative stress induced by PM2.5, polymyxin B (PMB) and N-acetylcysteine (NAC) were used to neutralize the effect of the endotoxin and inhibit the production of ROS, respectively. The results showed endotoxin and ROS played important roles in PM2.5-induced immune response. This study suggests that PM2.5 from pig house is a significant risk for immune response in alveolar macrophages. (C) 2019 Elsevier Ltd. All rights reserved.
机译:牲畜舍中的细颗粒物(PM2.5)不仅有害于动物的健康和福利,而且有害于在其中工作的农民。作为大气环境中重要的污染源,PM2.5可能威胁公众健康。研究了从保育猪场收集的PM2.5。它包含各种形态的颗粒,内毒素的浓度高达681.80 EU / mg。为了研究保育猪舍PM2.5诱导免疫反应的能力,研究了猪肺泡巨噬细胞3D4 / 21细胞。结果表明,PM2.5可以通过激活TLR4 / MyD88途径和NLRP3炎性小体来诱导细胞死亡,ROS产生和炎性细胞因子释放(IL-1 beta,IL-18,TNF-α和COX-2)。此外,TLR4 / MyD88,MAPK和NF-κB的下游信号通路参与了NLRP3炎性体的激活。为了进一步研究内毒素在PM2.5中的作用以及PM2.5诱导的氧化应激,使用了多粘菌素B(PMB)和N-乙酰半胱氨酸(NAC)来中和内毒素的作用并抑制ROS的产生,分别。结果表明内毒素和ROS在PM2.5诱导的免疫反应中起重要作用。这项研究表明,来自猪舍的PM2.5对肺泡巨噬细胞的免疫反应具有重大风险。 (C)2019 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Chemosphere》 |2019年第12期|124373.1-124373.12|共12页
  • 作者单位

    Nanjing Agr Univ Coll Anim Sci & Technol 1 Weigang Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Coll Anim Sci & Technol 1 Weigang Nanjing 210095 Jiangsu Peoples R China|Nanjing Agr Univ Coll Anim Sci & Technol Natl Expt Teaching Demonstrat Ctr Anim Sci Nanjing 210095 Jiangsu Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    PM2.5; Pig house; Alveolar macrophages; Oxidative stress; Endotoxin;

    机译:PM2.5;猪房肺泡巨噬细胞;氧化应激内毒素;

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