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Updated: Jun 13, 2026

Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice
Published on: September 19, 2019
Stimulating the central nervous system to prevent intestinal dysfunction after traumatic brain injury
Vishal Bansal1, Todd Costantini, Seok Yong Ryu
1Department of Surgery, Division of Trauma, Surgical Critical Care and Burns, University of California San Diego, California, USA.
Vagal nerve stimulation can prevent increased intestinal permeability after traumatic brain injury (TBI). This intervention also modulates gut inflammation and glial activity, suggesting a central nervous system role in gut barrier regulation.
Area of Science:
- Neuroscience
- Gastroenterology
- Trauma Research
Background:
- Traumatic brain injury (TBI) is known to cause gastrointestinal dysfunction and compromise the gut barrier.
- The central nervous system (CNS) may play a role in regulating gut barrier integrity following TBI.
- This study investigates the potential of vagal nerve stimulation (VNS) to mitigate TBI-induced increases in intestinal permeability.
Purpose of the Study:
- To determine if vagal nerve stimulation can prevent the increase in intestinal permeability after TBI.
- To assess the impact of VNS on inflammatory markers and glial activity in the ileum post-TBI.
- To explore the CNS-mediated mechanisms regulating the gut barrier after TBI.
Main Methods:
- Balb/c mice were subjected to a weight drop TBI model.
- Electrical stimulation of the cervical vagus nerve was applied before TBI in a subset of animals.
- Intestinal permeability was measured using FITC-Dextran, and ileum tissue was analyzed for tumor necrosis factor-alpha and glial fibrillary acidic protein (GFAP).
Main Results:
- TBI significantly increased intestinal permeability compared to sham controls (p < 0.01).
- Vagal nerve stimulation effectively prevented the TBI-induced rise in intestinal permeability (p < 0.02).
- VNS reduced intestinal tumor necrosis factor-alpha levels and altered glial fibrillary acidic protein expression in the ileum following TBI.
Conclusions:
- Vagal nerve stimulation is effective in preventing TBI-induced intestinal hyperpermeability in a mouse model.
- VNS appears to modulate gut inflammation and enhance enteric glial activity.
- These findings suggest that the vagus nerve serves as a critical pathway for CNS regulation of the gut barrier after TBI.
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