An imbalance in ligands, which are molecules produced by the body and the gut microbiota, can affect a key receptor protein that plays a role in brain inflammation after stroke, according to researchers.
The researchers at UTHealth Houston studied host-derived ligands, those produced by the host body, and microbiota-derived ligands, which are produced only by gut microbiota fermentation.
Both of the ligand types affect the aryl hydrocarbon receptor (AHR), which is involved in immune regulations and inflammation.
After a stroke, a metabolite called kynurenine, a host-derived ligand for AHR, increases. Meanwhile, stroke-induced dysbiosis – disruption of the gut microbiota – can lead to a loss of microbiota-derived ligands, which in turn would have a negative effect on the balance of AHR signalling.
“This study looked at how substances from the body and gut bacteria called AHR ligands affect post-stroke inflammation,” said senior author Bhanu Priya Ganesh, associate professor of neurology with McGovern Medical School at UTHealth Houston.
“They found that after a stroke, changes in gut bacteria lead to a drop in beneficial substances and an increase in harmful ones. This suggests that restoring these beneficial substances from gut bacteria could help reduce inflammation after a stroke.”
Previous UTHealth Houston preclinical, animal-model research showed that stroke and neurodegenerative diseases create systemic responses in which the gut microbiota plays a key role, and aging worsened stroke-induced dysbiosis.
“Our recent animal-model study points to new treatment options that could focus on the gut-brain connection, offering potential ways to improve recovery after a stroke and reduce brain damage,” Ganesh said.
