Oral ingestion of the environmental toxicant trichlorethylene in
rats induces alterations in the gut microbiome: relevance to
idiopathic Parkinson’s disease

Microbial alterations within the gut microbiome appear to be a common feature of individuals with Parkinson’s
disease (PD), providing further evidence for the role of the gut-brain axis in PD development. As a major site of
contact with the environment, questions have emerged surrounding the cause and effect of alterations to the gut
microbiome by environmental contaminants associated with PD risk, such as pesticides, metals, and organic
solvents. Recent data from our lab shows that ingestion of the industrial byproduct and environmental pollutant
trichloroethylene (TCE) induces key Parkinsonian pathology within aged rats, including the degeneration of
dopaminergic neurons, α-synuclein accumulation, neuroinflammation, and endolysosomal deficits. As TCE is
the most common organic contaminant within drinking water, we postulated that ingestion of TCE associated
with PD-related neurodegeneration may alter the gut microbiome to a similar extent as observed in persons with
PD. To assess this, we collected fecal samples from adult rats treated with 200 mg/kg TCE over 6 weeks via oral
gavage and analyzed the gut microbiome via whole genome shotgun sequencing. Our results showed changes in
gut microorganisms reflective of the microbial signatures observed in individuals with idiopathic PD, such as
decreased abundance of short-chain fatty acid producing Blautia and elevated lactic-acid producing
Bifidobacteria, as well as genera who contain species previously reported as opportunistic pathogens such as
Clostridium. From these experimental data, we postulate that TCE exposure within contaminated drinking water
could induce alterations of the gut microbiome that contributes to chronic disease risk, including idiopathic PD. CLICK TO REVIEW