Published in the Journal of Neurotrauma, the paper describes the faecal microbiome of the chronic TBI group as having absent or reduced numbers of beneficial bacterial species with higher numbers of bacteria linked to amino acid deficiency.
“Mild TBI is associated with alterations in gut metabolism soon after injury with direct impacts upon the intestinal mucosa, including loss of tight junctions, that contribute to increased intestinal permeability, inflammation and malabsorption,” writes the team, headed up by Dr Randall Urban, Professor in the department of internal medicine at The University of Texas Medical Branch’s School of Medicine.
“Patients with mild TBI also can develop sequelae years after injury, presenting with profound fatigue and altered cognition. Such mucosal alterations likely foster dysbiotic conditions to which the intestinal microbiota adapt, ultimately establishing an altered bacterial population that propagates the sequelae.”
In the trial, faecal microbiome profiles of 22 moderate/severe TBI were compared to 18 healthy age-matched control subjects.
Each faecal microbiome was characterised via gene sequencing and metagenomic genome sequencing approaches.
Main findings revealed that the faecal microbiome of the chronic TBI group had absent or reduced Prevotella spp. and Bacteroidies spp.
In contrast bacteria in the Ruminococcaceae family were higher in abundance in TBI compared to control profiles.
The paper referred to a previous study that reported significantly reduced levels of the amino acids tryptophan, l-sarcosine, ß-alanine, and alanine, positively correlated with reduced levels of Prevotella spp. in the TBI group samples vs. controls.
“Decreased post-meal amino acid levels of the TBI patients in our cohorts support the idea that the intestinal microenvironment also would have altered amino acid metabolism,” suggests the researchers.
“Unknown mechanisms may be selecting for bacteria that carry necessary machinery to compensate for amino acid deficits, adds the scientific team, which includes colleagues from the University of Newcastle, UK.
Metabolic and inflammatory link
In a discussion last month, Dr Urban and fellow team member Dr Melinda Sheffield-Moore, highlighted TBI impact on the gut-brain axis in a 2017 study identifying a possible metabolic and inflammatory link.
“It’s not clear why certain individuals appear more susceptible than others to developing persistent problems following TBI such as fatigue and brain fog.
“A growing body of evidence suggests that gut bacterial communities contribute to human physiology, immunity and inflammation, and dysbiosis of these communities can affect cognition, behaviour and mood.
“We and others believe that TBI-induced changes to the gut microbiome lead to alterations in gut metabolism, including altered production of short-chain fatty acids, and intestinal mucosa resulting in potential disruption of the gut-brain axis.”
The two researchers thought the results may discover potential therapeutic and mechanistic insights into chronic TBI that could eventually lead to the replacement of the dysbiotic intestinal community by faecal microbiome transplant to improve symptoms.
Source: Journal of Neurotrauma
Published online: doi.org/10.1089/neu.2019.6688
“Altered Faecal Microbiome Years after Traumatic Brain Injury.”
Authors: Randall Urban et al.