Scientists have uncovered a two-way link between traumatic brain injury (TBI) and intestinal changes.

These interactions may contribute to increased infections in patients, and could also worsen chronic brain damage, say US researchers.

A study by the University of Maryland School of Medicine (UMSOM) found that TBI in mice can trigger delayed, long-term changes in the colon; and that subsequent bacterial infections in the gastrointestinal system can increase posttraumatic brain inflammation and associated tissue loss.

TBI’s significant effect on the gastrointestinal tract is well evidenced. Until now, however, scientists have not recognised 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.

It is not clear how TBI causes these gut changes. A key factor in the process may
be enteric glial cells (EGCs), a class of cells that exist in the gut.

These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. Following TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain.

Researchers don’t know whether activation of EGCs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

TBI reportedly makes people 12 times more likely to die from blood poisoning, which is o en caused by bacteria.

They are also 2.5 times more likely to die of a digestive system problem, compared to those without such injury, according to data cited by UMSOM.

Trauma professor and lead researcher Alan Faden said: “These results indicate strong two-way interactions between the brain and the gut that may help to explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches.”

The researchers also focused on how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli. In mice with a TBI who were infected, brain inflammation worsened.

Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection.

This suggests that TBI may trigger a vicious cycle, in which brain injury causes gut dysfunction, which then has the potential to worsen the original brain injury.