Traumatic brain injury causes intestinal damage

Researchers has found a two-way link between traumatic brain injury (TBI) and intestinal changes. These interactions may contribute to increased infections and may worsen chronic brain damage. This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase post traumatic brain inflammation and associated 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. TBI has significant effects on the gastrointestinal tract, 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.

People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma. 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. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don't know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

The researchers also focused on the two-way nature of the process: 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, which infects humans. In mice with a TBI who were infected with the bacteria, 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.
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Smoking may cause inflammatory bowel disease

Exposing mice to cigarette smoke results in colitis, an inflammation of the colon resembling Crohn's disease, and identify a specific white blood cell and inflammatory protein responsible for this effect. Previous research shows that smoking significantly increases the risk of Crohn's disease, an inflammatory bowel disease. However the mechanism by which cigarette smoke affects the gastrointestinal system was not known.

One possibility is that inflammation in the lungs caused by smoking could have a knock-on effect in the intestine.
a connection between the lung and the large intestine has long been emphasized. Crohn's disease may occur in people with airway diseases, suggesting that inflammation in the lungs is linked with inflammation in the gut.

Researchers exposed mice to smoke from twenty cigarettes a day, six days a week, for a few weeks. The researchers then examined the presence of inflammation in the mice's lungs and colons. Mice exposed to cigarette smoke showed significant inflammation in their lungs. Interestingly, they also suffered from a type of colitis resembling Crohn's disease.

The researchers found increased levels of mucus and inflammation in the colon, and blood in the feces of the smoke-exposed mice. They also found increased levels of CD4+ T cells, a type of white blood cell, which were releasing a pro- inflammatory protein called interferon-gamma. Cigarette smoking activates specific white blood cells in the lung, which might move to the colon, triggering bowel inflammation.
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