This marks the first time that an observed permeability change has occurred in the gut due to brain injury.
Alan Faden, MD
Researchers at the University of Maryland School of Medicine have unearthed 2-way link that associates traumatic brain injury with changes in the intestines.
Led by Alan Faden, MD, the David S. Brown professor in trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at the University of Maryland, the team found that traumatic brain injury in mice can trigger long-term, but delayed, changes in the colon. These changes can then directly impact bacterial infections within the gastrointestinal system, resulting in an increase in post-traumatic brain inflammation and 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,” Faden said in a statement.
While the knowledge of a link between traumatic brain injury and the gastrointestinal tract has existed for years, this marks the first time that an observed permeability change has occurred in the gut due to brain injury.
The study examined mice given a controlled cortical impact (CCI) and observed the changes in the intestinal tract over a 28-day period. Although it is still unclear how the brain injury causes these changes, the process is believed to be related to enteric glial cells (EGCs), which are similar to the astroglial cells that exist in the brain. Both of which are activated after traumatic injury to the brain.
That activation is associated with brain inflammation which contributes to delayed tissue damage, although the investigators are unsure if whether the ECG activation is the body’s attempt to compensate for injury to the brain, or if it is contributing to the intestinal injury.
Researchers found that 28 days post controlled cortical impact, there was increased paracellular permeability and a decrease in claudin-1 mRNA as well as protein expression in the colon. In addition, colonic glial cell GFAP and Sox10 expression were also increased.
The mice used in the study were tested for Citrobacter rodentium (Cr), the rodent equivalent of an Escherichia Coli (E. Coli) infection in a human. When the infection was present in mice post-CCI, their brain lesion injuries worsened, and their astrocyte- and microglial-mediated inflammation increased.
After traumatic brain injury, patients are 12 times more susceptible to mortality from blood poisoning and 2.5 times more likely to die from an issue with their digestive system, according to the investigators, because the brain injury allows more harmful microbes to leave the intestines and traverse other areas of the body.
The study, “Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice,” was published in Brain, Behavior, and Immunity.