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首页> 外文期刊>Brain research >Chronic colitis induces meninges traffic of gut-derived T cells, unbalances M1 and M2 microglia/macrophage and increases ischemic brain injury in mice
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Chronic colitis induces meninges traffic of gut-derived T cells, unbalances M1 and M2 microglia/macrophage and increases ischemic brain injury in mice

机译:慢性结肠炎诱导肠道衍生的T细胞的脑力流量,不平衡M1和M2小胶质细胞/巨噬细胞,并增加小鼠的缺血性脑损伤

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摘要

Ischemic stroke is one of the most common diseases leading to death and is the primary cause of physical handicap. Recent studies have reported that chronic colitis increases the risk of ischemic stroke, but it is unknown whether chronic colitis participates in ischemic brain injury directly. A combined mouse model of chronic colitis induced by dextran sodium sulfate (DSS) and ischemic stroke induced by photochemical infarction was used in this study. We demonstrated that chronic colitis significantly increased the infarction volume, activated microglia/macrophage numbers, proliferation of M1 microglia/macrophage, non-gut-derived CD4 + T lymphocyte penetration and decreased neuron numbers in the peri-infarction at 7 d after stroke. Furthermore, gut derived CD4 + T cell accumulation on the meninges was observed at 7 d after stroke. In addition, selective depletion of meningeal macrophages resulted in a reduction of infarction volume and the non-gut-derived CD4 + T lymphocyte penetration. We concluded that chronic colitis exacerbated ischemic stroke by promoting CD4 + T cell migration from the gut to the meninges and disequilibrium of M1 and M2 microglia/macrophages. We speculated that the gut-derived CD4 + T cells may interact with meningeal macrophages and result in non-gut derived CD4 + T lymphocyte infiltration that aggravated brain injury in ischemic stroke.
机译:缺血性卒中是导致死亡的最常见疾病之一,是物理障碍的主要原因。最近的研究报道说,慢性结肠炎增加了缺血性卒中的风险,但慢性结肠炎是否直接参与缺血性脑损伤是未知的。本研究使用了由光化学梗死诱导的葡聚糖硫酸钠(DSS)诱导的慢性结肠炎的组合小鼠模型。我们证明,慢性结肠炎显着增加了梗死体积,活性微胶质细胞/巨噬细胞的增殖,M1微胶质瘤/巨噬细胞,非肠道衍生的CD4 + T淋巴细胞渗透率,卒中后7d在7d中的PERI梗死中的神经元数减少。此外,在中风后7 d观察到脑膜肠道衍生的CD4 + T细胞积累。此外,选择性耗竭脑膜巨噬细胞导致梗死体积和非肠道衍生的CD4 + T淋巴细胞渗透率降低。我们得出结论,慢性结肠炎通过促进从肠道与M1和M2微胶质细胞/巨噬细胞的脑膜和不平衡的CD4 + T细胞迁移而加剧了缺血性卒中。我们推测肠道衍生的CD4 + T细胞可以与脑膜巨噬细胞相互作用,导致非肠道衍生的CD4 + T淋巴细胞浸润,该缺血中脑损伤加剧。

著录项

  • 来源
    《Brain research》 |2019年第2019期|共10页
  • 作者单位

    Sun Yat Sen Univ Affiliated Hosp 5 Dept Neurol Zhuhai 519000 Peoples R China;

    Sun Yat Sen Univ Affiliated Hosp 1 Dept &

    Key Discipline Neurol Dept Neurol Natl Key Clin;

    Sun Yat Sen Univ Affiliated Hosp 5 Dept Neurol Zhuhai 519000 Peoples R China;

    Sun Yat Sen Univ Affiliated Hosp 5 Dept Neurol Zhuhai 519000 Peoples R China;

    Sun Yat Sen Univ Affiliated Hosp 1 Dept &

    Key Discipline Neurol Dept Neurol Natl Key Clin;

    Sun Yat Sen Univ Affiliated Hosp 1 Dept &

    Key Discipline Neurol Dept Neurol Natl Key Clin;

    Sun Yat Sen Univ Affiliated Hosp 5 Dept Neurol Zhuhai 519000 Peoples R China;

    Sun Yat Sen Univ Affiliated Hosp 1 Dept &

    Key Discipline Neurol Dept Neurol Natl Key Clin;

    Sun Yat Sen Univ Affiliated Hosp 5 Dept Neurol Zhuhai 519000 Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经病学;
  • 关键词

    Chronic colitis; Ischemic brain injury; M1/M2; Microglia/macrophage; CD4+T lymphocyte; Meningeal macrophages;

    机译:慢性结肠炎;缺血性脑损伤;m1 / m2;microglia /巨噬细胞;cd4 + t淋巴细胞;脑膜巨噬细胞;

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