Last updated April 18, 2018 at 9:22 am
The body’s defences against infection could also help mend physical damage to brain tissue, a new study has found.
“The lining of the brain, with help from the immune system, has a remarkable ability to put itself back together again after injury,” said Dorian McGavern, who led research by the National Institutes of Health.
“As we learn more about all the cells involved in the repair process, we may be able to identify potential targets for therapy that lead to better outcomes for patients.”
As a layer of membranes that line the main organs of the central nervous system, the meninges are responsible for protecting the brain and spinal cord tissues from physical injury. Damage to such a complicated network can cause cell death in underlying brain tissue.
But the study at the NIH’s National Institute of Neurological Disorders and Stroke showed that, in mice, immune cells assisted with restoring the damaged brain lining to fully functioning capacity.
The first defence
On the first day of injury, inflammatory monocytes – or white blood cells – were sent directly to the injured meningeal tissue to remove dead cells. A few days later, these immune cells were helped by other blood monocytes that condensed around the edges of the legion to rebuild damaged blood vessels.
Within a week, the team found that the tasks completed by these immune cells were scheduled and undertaken one after the other, with no overlap or competition.
“Following a head injury, the meninges call in a clean-up crew, followed by a separate repair crew, to help fix damaged blood vessels,” said Dr McGavern.
Time after time
The timing of a second brain injury also influenced the repair process of the meninges in the affected mice. Another injury experienced within one day of the first traumatic brain injury resulted in more inflammation, and an absent repairing of blood vessels. Yet if the second injury occurred after this wound healing phase has already started, the repair process went on as normal.
“We have shown on a cellular level, that two or more head injuries within a very short amount of time can have really dire consequences for the brain lining and its ability to repair,” said McGavern.
“It is possible that patients who did not fully recover following a head injury may have had problems with the first phase of the repair process.”
With advanced imaging tools and various experiments, it was revealed that the molecule matrix metalloproteinase 2 (Mmp2) could potentially have a vital role in blood vessel restoration. This second wound-healing release of Mmp2 breaks down the matrix which holds cells together, creating space for new blood vessels. Blocking the molecule therefore led to limited vessel repair.
The team were intrigued by the results of a previous study on MRI scans of concussions and Mild Traumatic Brain Injury (MTBI) in adult patients, with half of the scans showing blood vessel damage in the meninges. While most brains had repaired blood vessels within 20 days, 17 per cent still showed damage three months after injury. This demonstrated ongoing damage to the meninges and incomplete recovery processes.
From this study, a broader understanding of meningeal healing and the effects of repetitive brain damage allows researchers to perhaps discover other molecules and genes involved in brain repair and identify other ways to accelerate recovery after a head injury.
The study was published in Nature Immunology.