Summary: Scientists have discovered a “neurobiotic sense”—a newly identified system in which the gut sends real-time signals from microbes to the brain to help regulate appetite. Specialized cells called neuropods in the colon detect a bacterial protein, flagellin, and signal the brain via the vagus nerve to suppress eating.
Mice lacking the receptor for this signal continued to eat and gain weight, highlighting the pathway’s role in appetite control. This advance suggests that our gut microbes can directly influence behavior and opens avenues for studying diet, obesity, and mood disorders.
Key facts:
Neuropods detect gut microbes and signal the brain to regulate appetite.
The bacterial protein flagellin triggers this real-time gut-brain communication.
Disrupting the pathway alters eating behavior and weight gain in mice.
Source: Duke University
In a breakthrough that reimagines how the gut and brain communicate, researchers have discovered what they call the “neurobiotic sense,” a newly identified system that allows the brain to respond in real time to signals from microbes living in our gut.
The new research, led by Duke University School of Medicine neuroscientists Diego Bohórquez, PhD, and M. Maya Kaelberer, PhD, and published in Nature, focuses on neuropods, tiny sensor cells that line the colon’s epithelium. These cells detect a common microbial protein and send rapid messages to the brain that help curb appetite.
But this is just the beginning. The team believes this neurobiotic sense could be a broader platform for understanding how the gut detects microbes, influencing everything from eating habits to mood—and even how the brain can shape the microbiome in return.
“We were curious to know if the body could detect microbial patterns in real time, not just as an immune or inflammatory response, but as a neural response that guides behavior in real time,” said Bohórquez, professor of medicine and neurobiology at Duke University School of Medicine and senior author of the study.
The key player is flagellin, an ancient protein found in bacterial flagella, a tail-like structure that bacteria use to swim. When we eat, some gut bacteria release flagellin. Neuropods detect it, with the help of a receptor called TLR5, and trigger a message through the vagus nerve—a key communication line between the gut and the brain.
The team, supported by the National Institutes of Health, proposed a bold idea: that bacterial flagellin in the colon could trigger neuropods to send an appetite-suppressing signal to the brain—a direct microbial influence on behavior.
The researchers tested this by fasting mice overnight, then giving them a small dose of flagellin directly to the colon. Those mice ate less.
When the researchers tried the same experiment in mice without the TLR5 receptor, nothing changed. The mice continued eating and gained weight, a clue that the pathway helps regulate appetite.
The findings suggest that flagellin sends a “we’ve had enough” signal through TLR5, allowing the gut to tell the brain it’s time to stop eating. Without this receptor, the message doesn’t get through.
The discovery was led by the study’s lead authors, Winston Liu, MD, PhD, Emily Alway, both graduate students in the Medical Scientist Training Program, and postdoctoral fellow Naama Reicher, Ph.D.
Their experiments reveal that disrupting the pathway altered eating habits in mice, pointing to a deeper link between gut microbes and behavior.
“Looking ahead, I think this work will be especially useful for the broader scientific community in explaining how our behavior is influenced by microbes,” said Bohórquez.
“A clear next step is to investigate how specific diets change the microbial landscape in the gut. This could be a key piece of the puzzle in conditions like obesity or psychiatric disorders.”
