Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in trauma patients. The primary focus of treating TBI is to prevent additional injury to the damaged brain tissue, known as secondary brain injury. This treatment can include treating the body’s inflammatory response. Despite promise in animal models, anti-inflammatory therapy has failed to improve outcomes in human patients, suggesting a more targeted and precise approach may be needed. There is a bidirectional axis between the intestine and the brain that contributes to this inflammation in acute and chronic injury. The mechanisms for this interaction are not completely understood, but there is evidence that neural, inflammatory, endocrine, and microbiome signals all participate in this process. Therapies that target the intestine as a source of inflammation have potential to lessen secondary brain injury and improve outcomes in TBI patients, but to develop these treatments we need to better understand the mechanisms behind this intestinal inflammatory response.

创伤性脑损伤 (TBI) 是创伤患者发病率和死亡率的重要原因。治疗 TBI 的主要重点是防止对受损脑组织的额外伤害，称为继发性脑损伤。这种治疗可以包括治疗身体的炎症反应。尽管在动物模型中有希望，但抗炎治疗未能改善人类患者的预后，这表明可能需要更有针对性和更精确的方法。肠道和大脑之间有一个双向轴，在急性和慢性损伤中会导致这种炎症。这种相互作用的机制尚不完全清楚，但有证据表明神经、炎症、内分泌和微生物组信号都参与了这一过程。