![]() One group of proteins released after viral infection are called type I interferons (IFN-I), which turn on a variety of genes that affect the immune response. When cells in the body become infected, they call for help by releasing proteins that signal the immune system. These findings highlight the utmost importance in quickly identifying and treating infections in patients.”Īlthough the presence of infection was affecting the immune system’s ability to respond to mTBI, the exact cause remained unknown. “In the case of mild TBI, this seems to be ok, but when you have a large vascular injury in the brain itself, like a stroke, every minute counts. “The presence of infection causes the immune system to take a break from repair while it fights off the virus,” said Dr. The repaired brain blood vessels, which are normally very well sealed, remained permanently leaky. This timing is especially critical in the case of CVI mice, because the delay in response produced by infection led to permanent cognitive dysfunction and damage to the brain tissue. This change in priority for the immune system is not permanent, as infected mice were able to eventually repair the blood vessel damage at a later time compared to uninfected mice, unless a second infection was encountered. ![]() ![]() “Because the body is dealing with a greater threat, cells that would normally repair the damaged blood vessels in or around the brain are needed elsewhere.” “Evolution prioritizes mobilizing the immune system to fight off infection over repair,” said Dr. The study also looked in a second injury model affecting the blood vessels in the brain, called a cerebrovascular injury (CVI), and saw a similar effect on repair. When they looked closer, they observed that some cells of the immune system no longer moved into the site of the injury, which occurred in the uninfected animals, suggesting they were responding to systemic infection. Making use of a mouse model for mild TBI (mTBI) that they had developed previously, the team of researchers led by NINDS scientist Dorian McGavern, Ph.D., discovered that viral, fungal, or a mimic for bacterial infections all impacted blood vessel repair within the meninges, the protective covering of the brain. The findings were published in Nature Immunology. Researchers at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, have found a possible explanation for why some patients recover much more poorly from brain injury if they later become infected. Traumatic brain injury (TBI) and other injuries to blood vessels in the brain, like stroke, are a leading cause of long-term disability or death. A marker for intact vessels was used (labeled in green) to distinguish fully functional blood vessels (yellow) from ones that are still damaged (red). Viral Infection Slows Blood Vessel Repair After TBI: Seven days after mTBI, the blood vessels (stained in red) in the tissues around the brain are not completely repaired.
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