What if healing the brain after traumatic injury starts in the gut?
In a new study published in Nature Communications Biology , Houston Methodist researchers led by Sonia Villapol, Ph.D. , found that short-term antibiotic treatment significantly reduced neuroinflammation and neurodegeneration following traumatic brain injury (TBI) by altering the gut microbiome in animal models.
"We found that antibiotic treatment following TBI can reduce harmful gut bacteria, decrease lesion size and limit cell death," said Villapol, an associate professor in the Department of Neurosurgery at Houston Methodist. "Our results support a gut–brain mechanism in which microbiome changes influence peripheral immunity and, in turn, neuroinflammation after TBI.¨
Administering antibiotics cleans the gut of harmful bacteria, allowing beneficial bacteria to flourish. The study found that two helpful bacteria, Parasutterella excrementihominis and Lactobacillus johnsonii, are key to driving cell repair. According to Villapol, they could also be major regulators for peripheral inflammation in the body.
Notably, 70% of immune system regulation is generated by the gut microbiome. During gut imbalance, the bidirectional nature of the brain-gut axis can wreak havoc throughout the entire body.
"Our brains are constantly sending signals to the rest of our bodies. Following a traumatic brain event, those signals can get scrambled and disrupt other organs, including our digestive system," Villapol said. "If the gut stays out of balance, the brain may have a harder time healing."
There are an estimated 4 million traumatic brain injuries a year in the U.S. Recent studies indicate that TBI-induced gut microbiome imbalance may even contribute to the development of neurodegenerative diseases like Parkinson's, Alzheimer's and dementia.
Villapol's lab is focused on investigating and developing new neuroprotective treatments to fight inflammation linked with neurodegenerative disease. "If we can break neuroinflammation in the acute or chronic stage, we can reduce the risk of developing Alzheimer's or dementia," Villapol said.
The next phase of the research will focus on bioengineering Parasutterella excrementihominis and Lactobacillus johnsonii to further develop precision therapies to reduce neuroinflammation.
Other collaborators in the study include Hannah Flinn, Austin Marshall, Morgan Holcomb, Marissa Burke, Goknur Kara, Leonardo Cruz-Pineda, Sirena Soriano and Todd J. Treangen.
This work was supported in part by grants from Houston Methodist Research Institute and the National Institutes of Health (NIH).
