Summary: Study reveals a causal mechanism for pain reduction may be due to an antibiotic-induced shift in the gut’s amino acid concentrations.
Source: University of New England
Glenn Stevenson, Ph.D., professor of psychology within the School of Social and Behavioral Sciences at UNE, recently published a paper on gut microbiome modulation of inflammatory pain.
The paper, “Effects of vancomycin on persistent pain-stimulated and pain-depressed behaviors in female Fischer rats with or without voluntary access to running wheels,” was published in The Journal of Pain.
The research paper examines the impact of antibiotics on the gut microbiome and how antibiotic use can alter inflammatory pain in subjects with or without access to exercise.
According to Stevenson, this is the first publication to assess how antibiotic-induced changes to the gut microbiome impact inflammatory pain distal to the gut (in the limbs, for example), using behavioral procedures developed in the Stevenson Lab.
Results from this study indicate that the glycopeptide antibiotic vancomycin decreases pain-related behaviors and that manipulation of the gut microbiome may be one method to attenuate inflammatory pain amplitude. Additionally, results indicated that a causal mechanism for this reduction in pain may be due to an antibiotic-induced shift in gut amino acid concentrations.
The research for this study took four years to complete, Stevenson said, adding that the link between amino acids and pain reduction is “highly novel.”
“This is another example of the high-quality, high-impact research that our UNE undergraduate students are engaged in daily,” Stevenson said. “These co-authorships go a long way toward securing post-graduate positions for our students.”
Stevenson also spoke of the interprofessional nature of the research.
“This publication represents a highly interdisciplinary research team with expertise in genomics, proteomics, metabolomics, pharmacology, psychology, neuroscience, microbiology, and virology,” he commented.
“When you put all these disciplines together to solve a single problem, you end up doing innovative, creative, and significant work. The main ideas for this research were generated in meetings between me, Meghan [May] and Tamara [King]. I then reached out to Penn and Children’s Hospital researchers who subsequently joined our group, and the rest is history.”
Effects of Vancomycin on Persistent Pain-Stimulated and Pain-Depressed Behaviors in Female Fischer Rats With or Without Voluntary Access to Running Wheels
The present experiments determined the effects of the narrow-spectrum antibiotic vancomycin on inflammatory pain-stimulated and pain-depressed behaviors in rats. Persistent inflammatory pain was modeled using dilute formalin (0.5%).
Two weeks of oral vancomycin administered in drinking water attenuated Phase II formalin pain-stimulated behavior, and prevented formalin pain-depressed wheel running. Fecal microbiota transplantation produced a non-significant trend toward reversal of the vancomycin effect on pain-stimulated behavior.
Vancomycin depleted Firmicutes and Bacteroidetes populations in the gut while having a partial sparing effect on Lactobacillus species and Clostridiales. The vancomycin treatment effect was associated with an altered profile in amino acid concentrations in the gut with increases in arginine, glycine, alanine, proline, valine, leucine, and decreases in tyrosine and methionine.
These results indicate that vancomycin may have therapeutic effects against persistent inflammatory pain conditions that are distal to the gut.
The narrow-spectrum antibiotic vancomycin reduces pain-related behaviors in the formalin model of inflammatory pain. These data suggest that manipulation of the gut microbiome may be one method to attenuate inflammatory pain amplitude.