Brain injuries may be causing problems elsewhere in the body.

Researchers from the University of Maryland School of Medicine (UMSOM) have discovered a two-way link between traumatic brain injuries (TBI) and intestinal changes that may contribute to increased infections in patients, and could also worsen chronic brain damage.

“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,” lead researcher, Dr. Alan Faden, 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, said in a statement.

In the study, the researchers found that TBI in mice can trigger delayed, long-term changes in the colon and subsequent bacterial infections in the gastrointestinal system can increase posttraumatic brain inflammation and associated tissue loss.

After examining mice that received an experimental TBI, the researchers found that the intestinal wall of the colon became more permeable after trauma, changes that were sustained over the following month.

Scientists have long known that TBI has significant effects on the gastrointestinal tract. However, it wasn’t known until now that brain trauma can make the colon more permeable, potentially allowing harmful microbes to migrate from the intestine to other areas of the body, causing infection.

However, the researchers do not fully know how TBI causes the gut changes. A crucial factor in the process could be enteric glial cells (ECG)—a class of cells that exist in the gut that are similar to brain astroglial cells.

After a brain injury, the activation is associated with brain inflammation that contributes to delayed tissue damage in the brain.

However, it is unknown whether the activation of ECGs after TBI contributes to intestinal injury or is an attempt to compensate for the injury.

During the study, the researchers also examined the two-way nature of how gut dysfunction may worsen brain inflammation and tissue loss after TBI. After infecting the mice with Citrobacter rodentium—a species of bacteria that is the rodent equivalent of E. coli—they found that brain inflammation worsened.

The mice also lost more neurons in the hippocampus than the animals without the infection.

The results suggest that TBI may trigger a cycle where brain injuries cause gut dysfunction, which then has the potential to worsen the original brain injury.

“These results really underscore the importance of bi-directional gut-brain communication on the long-term effects of TBI,” Faden said.