Long School of Medicine, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas.
Division of Trauma and Emergency Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Shock. 2019 Sep;52(3):318-325. doi: 10.1097/SHK.0000000000001278.
Traumatic brain injury (TBI) contributes to nearly 1 in 3 injury-related deaths in the United States and accounts for a substantial public health burden and cost. The current literature reports that physiologic responses in the gastrointestinal system after TBI include, but are not limited to, epithelial barrier dysfunction, microbiota changes, and immunologic transformations. Recent evidence suggests gut alterations after TBI modify the homeostasis of the bidirectional gut-microbiota-brain axis, resulting in altered immune responses in the periphery and the brain. This cascade possibly contributes to impaired central nervous system (CNS) healing. Although attention to the gut-brain-microbiota axis has been increasing in the literature, the precise mechanisms underlying the changes observed after TBI remain unclear. The purpose of this review are to describe our current understanding regarding alterations to the gut-microbiota-brain axis after TBI, highlight the pathophysiologic changes involved, and evaluate how these variations modify healing in the CNS or even contribute to secondary injury. We also discuss current investigations into potential medical therapies directed at the gut-microbiota-brain axis, which might offer improved outcomes after TBI.
创伤性脑损伤 (TBI) 导致美国近 1/3 的与损伤相关的死亡，造成了巨大的公共卫生负担和成本。目前的文献报道，TBI 后胃肠道系统的生理反应包括但不限于上皮屏障功能障碍、微生物群变化和免疫转化。最近的证据表明，TBI 后的肠道改变改变了双向肠道-微生物群-脑轴的内稳态，导致外周和大脑的免疫反应改变。这种级联反应可能导致中枢神经系统 (CNS) 愈合受损。尽管文献中对肠道-脑-微生物群轴的关注日益增加，但 TBI 后观察到的变化的确切机制仍不清楚。本综述旨在描述我们目前对 TBI 后肠道-微生物群-脑轴改变的理解，强调涉及的病理生理变化，并评估这些变化如何改变中枢神经系统的愈合，甚至导致继发性损伤。我们还讨论了针对肠道-微生物群-脑轴的潜在医学治疗的当前研究，这些治疗可能会提高 TBI 后的治疗效果。
