Brain injury can cause intestinal damage, which exacerbates brain inflammation.
In recent years, it’s become increasingly apparent that there is a bidirectional feedback loop commonly referred to as the “gut-brain axis” (or microbiome–gut–brain axis) that facilitates two-way communication between the gastrointestinal tract and the brain.
Gut-brain communication relies on afferent and efferent pathways of the vagus nerve and other mechanisms to send signals from "gut-to-brain" and "brain-to-gut." Bidirectional gut-brain interactions help to regulate homeostasis, immune responses, and inflammation.
It's important to emphasize that the human gut-brain axis is far from being fully understood. Disruptions of the gut-brain axis are associated with a diverse spectrum of maladies that include Parkinson’s disease, anxiety disorders, depression, and irritable bowel syndrome (IBS). However, the vast majority of research to date on the gut-brain axis has been conducted on animal models and much more human research is needed.
That being said, this week, the University of Maryland School of Medicine (UMSOM) announced that a research team led by Alan Faden has discovered a two-way correlation between traumatic brain injury (TBI) and intestinal changes in mice that are influenced by bidirectional gut-brain interactions. These findings were recently published in the journal Brain, Behavior, and Immunity.
This study is the first to identify that TBI in mice can trigger a vicious cycle in which a traumatic brain injury causes gut dysfunction. These gut disruptions exacerbate the original brain injury by causing inflammation, which further worsens gut dysfunction. And so on, and so on...This vicious cycle has the potential to snowball out of control.
More specifically, the UMSOM scientists found that TBI in mice caused changes in the GI tract that made the colon more permeable. This permeability increased the odds of harmful microbes migrating from the GI tract to other parts of the body and causing infection. Bacterial infections emanating from the GI system increased brain inflammation and were linked to neuron loss in the hippocampus.
The authors point out that human patients are 12 times more likely to die from blood poisoning (which is generally caused by bacteria) after TBI. Additionally, patients with TBI are 2.5 times more likely to die of a digestive system problem, compared with those without traumatic brain injury.
For years, researchers have known that TBI influences the gastrointestinal tract. But, until now, scientists were unaware that brain trauma in mammals can make the colon more permeable. Unfortunately, it remains unclear exactly how and why traumatic brain injury causes these specific changes in the gut.
As part of their bidirectional gut-brain axis research, the UMSOM scientists also focused on how extreme gut dysfunction may worsen brain inflammation. To pinpoint gut-to-brain directional influences, Faden et al. infected mice with the rodent equivalent of E. coli, which is called "Citrobacter rodentium.” Notably, when mice were infected with a potent gut bacteria, brain inflammation worsened.
The authors sum up their findings in the study abstract: “These experimental studies demonstrate chronic and bidirectional brain-gut interactions after TBI, which may negatively impact late outcomes after brain injury.”
The senior researcher of this study, Alan Faden, is a professor in the departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the Center for Shock, Trauma and Anesthesiology Research. In a statement, Faden concluded:
“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. These results really underscore the importance of bi-directional gut-brain communication on the long-term effects of traumatic brain injury.”
Other authors from UMSOM involved in this research include first author Elise Ma, a doctoral student; Terez Shea-Donahue, professor of radiation oncology; Bogdan A. Stoica, associate professor of anesthesiology; and David J. Loane, associate professor of anesthesiology.
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