Link between stomach and brain could lead to dangerous “feedback loop” after TBI
Researchers from the University of Maryland School of Medicine say they’ve discovered a relationship between the brain and stomach that could reshape how we think about brain injuries.
According to the report published in the journal Brain, Behavior, and Immunity, a two-way relationship between traumatic brain injury (TBI) and intestinal changes may contribute to increased infections after brain injury or more severe brain damage.
In the animal study, the team says TBI was able to trigger delayed, long-term changes in the colon that create a feedback loop which can increase posttraumatic brain inflammation and brain tissue loss.
“These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches,” said the lead researcher, Alan Faden, MD, the David S. Brown Professor in Trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the UMSOM Shock, Trauma and Anesthesiology Research Center.
Medical professionals have long believed such a relationship between the brain and gut exists but were unable to tie down how exactly it functions. Now, the scientists say they have found that brain injury can cause thinning in the colon, potentially allowing dangerous microbes to travel from the intestine to other areas of the body, leading to infection. The finding may help explain why people are 12 times more likely to die from blood thinning after TBI, and 2.5 times more likely to die of a digestive system problem.
To discover this, the team examined mice which had been given TBI. What they found indicated that the intestinal wall of the colon becomes more permeable after trauma, and may stay this way for more than a month after the injury.
Taking this further, the team examined the reverse relationship by infecting the mice with Citrobacter rodentium, a species of bacteria. They found that the mice with TBI who were infected with this bacteria experienced worse brain inflammation and neuron loss compared to those without infection.
While these findings may provide more insight into the relationship between TBI and intestinal issues, it is still unclear exactly why or how TBI causes these changes in the gut. The researchers suggest one possibility is that enteric glial cells – a class of cells in the gut similar to the brain’s astroglial cells – may be activated after TBI. This could potentially contribute to delayed tissue damage in both the brain and stomach.
“These results really underscore the importance of bi-directional gut-brain communication on the long-term effects of TBI,” said Dr. Faden.