Gut Microbiome Promise Possible Cure for Brain Inflammatory Disorders

text-align: center;">Gut Microbiome Promise Possible Cure for Brain Inflammatory Disorders

Microglia and astrocytes regulate inflammation and neurodegeneration in the central nervous system (CNS).  Microglia modulate pro-inflammatory and neurotoxic actions in astrocytes, but the mechanisms involved aren’t completely understood.

“For the first time, we’ve been able to identify that food has some sort of remote control over central nervous system inflammation,” said Francisco Quintana, an investigator in the Ann Romney Center for Neurologic Diseases at BWH and corresponding author on the study.

“What we eat influences the ability of bacteria in our gut to produce small molecules, some of which are capable of traveling all the way to the brain. This opens up an area that’s largely been unknown until now: how the gut controls brain inflammation. We essentially discovered a remote control by which the gut flora can control what is going on at a distant site in the body, in this case the central nervous system.”

Previous investigations have indicated a relation between the gut microbiome and brain inflammation, however both are connected and how dietary and diet products affect their relationship has remained mostly unknown.

In order to go a step further in this area, Quintana and colleagues conducted genome-wide transcriptional investigations on astrocytes- the star-shaped cells which live in the brain and spinal cord- at a mouse model of MS, differentiating a molecular pathway involved in inflammation.

They discovered that compounds derived from dietary tryptophan (an amino acid famously found in fish and other foods) behave with this pathway, which when more of those molecules are found, astrocytes can restrict brain inflammation.  In blood samples from MS patients, the group found levels of the molecules.

“Deficits in the gut flora, deficits in the diet or deficits in the ability to uptake these products from the gut flora or transport them from the gut — any of these may lead to deficits that contribute to disease progression,” said Quintana.

The team is keen to further explore exactly which bacterial metabolites affect the microglial inflammatory pathway and test the same in humans in an attempt to figure out more about how this lab-based research will translate to people with MS.

“Our study identified pathways that can be modulated in MS and we are working on tools for this. Currently, we are in the process of securing intellectual property agreements and also developing potential probiotic supplements with pharma companies,” Quintana concludes.