• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>British journal of neurosurgery >The role of vagus nerve overactivity in the increased incidence of pneumonia following traumatic brain injury
【24h】

The role of vagus nerve overactivity in the increased incidence of pneumonia following traumatic brain injury

机译：迷走神经过度活动在脑外伤后肺炎发病率增加中的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Nosocomial infections, pneumonia in particular, are well-known complications of traumatic brain injury (TBI), which are associated with a worse neurological outcome. This review aims to explore the role of vagus nerve activity in immunomodulation as a causative factor. A MEDLINE search revealed numerous reports published over the last decade describing the "cholinergic anti-inflammatory pathway" between the vagus nucleus and leukocyte activity. Using a combination of lipopolysaccharide stimulation and vagotomy, it has been shown that the parasympathetic fibres terminating in the spleen reduce tumour necrosis factor production. Further pharmacological and receptor knockout studies have identified the α7 subtype of nicotinic receptors as the likely target for this. Vagal activity also induces changes in neutrophil chemotaxis through altered expression of the CD11b integrin which is abolished by splenectomy. By extrapolating this evidence we suggest a possible mechanism for immunosuppression following TBI which also has the potential to be targeted to reduce the incidence of pneumonia. Whilst there is strong supporting evidence for the role of vagal nerve overactivity in post-TBI pneumonia, there have yet to be any clinical investigations and further study is required.
机译：医院感染，尤其是肺炎，是创伤性脑损伤（TBI）的众所周知的并发症，与神经功能恶化有关。这篇综述旨在探讨迷走神经活动在免疫调节中作为病因的作用。 MEDLINE搜索揭示了过去十年中发表的许多报告，描述了迷走神经核和白细胞活性之间的“胆碱能抗炎途径”。使用脂多糖刺激和迷走神经切断术的组合，已经表明终止于脾的副交感神经纤维减少了肿瘤坏死因子的产生。进一步的药理和受体敲除研究已确定烟碱样受体的α7亚型是可能的靶标。迷走神经活性还通过脾切除术消除的CD11b整联蛋白表达的改变来诱导中性粒细胞趋化性的变化。通过推断这一证据，我们建议在TBI后进行免疫抑制的一种可能的机制，该机制也有可能针对减少肺炎的发生。尽管有强有力的证据支持迷走神经过度活动在TBI后肺炎中的作用，但尚未进行任何临床研究，需要进一步的研究。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号