Exploring the “Brain–Gut–Microbiota Axis”: Dr. Gu Tingting’s Team Reveals How Stress Disrupts the Gut and the Mind

In the laboratory of the Department of Gastroenterology at Kawasaki Medical School, researcher Dr. Gu Tingting is closely examining a set of newly collected data. These results come from mice exposed to social defeat stress (SDS)—a well-established stress model now helping scientists answer a long-standing question: Why do gastrointestinal symptoms and emotional disturbances so often appear together under chronic stress?

At the 27th Annual Meeting of the Japanese Society of Neurogastroenterology, Dr. Gu presented her team’s latest findings, providing the first systematic map of how stress disrupts communication among the brain, gut, and gut microbiota. The work marks a meaningful breakthrough in understanding the mechanisms behind disorders of gut–brain interaction (DGBI), particularly irritable bowel syndrome (IBS).

IBS is a common functional gastrointestinal disorder defined by abdominal pain, bloating, and altered bowel habits—even though routine examinations seldom reveal structural abnormalities. For years, clinicians have relied on the concept of the gut–brain axis to explain how psychological stress triggers gut symptoms, but the underlying mechanisms have remained largely unclear. Dr. Gu’s study aims to illuminate this “black box.”

“Our goal is not only to examine the two-way dialogue between the brain and the gut,” she explained. “We want to clarify the crucial role played by gut microbiota. How does psychosocial stress disturb the microbial community, alter neurochemical signaling, and ultimately lead to gastrointestinal dysfunction and changes in mood? That is the question we set out to answer.”

The study shows that chronic stress sharply reduces several beneficial butyrate-producing bacteria—microbes that generate butyrate, a short-chain fatty acid essential for maintaining the gut barrier and regulating inflammation. When butyrate levels fall, the intestinal lining becomes more vulnerable. At the same time, bacteria that degrade the mucus layer increase, pushing the microbial ecosystem further out of balance.

These microbial shifts come with clear warning signs from the gut itself. Protective proteins that support the intestinal barrier decline, while inflammation-related factors rise. Multiple genes involved in gut motility and visceral sensitivity also undergo significant changes. Correspondingly, stressed mice display altered bowel function and abnormal fecal water content—classic features of IBS-like symptoms.

Stress also reshapes the brain. The team identified changes in several neuroreceptors within regions involved in emotional regulation, social behavior, and stress response. These include dopamine receptors, which influence reward and motivation, and oxytocin receptors—the so-called “trust hormone.” Such neural changes suggest that the brain undergoes stress-induced recalibration, helping explain why IBS patients often experience anxiety, depression, or sleep disturbances.

“This creates a typical vicious cycle,” Dr. Gu noted. “Stress reduces beneficial butyrate-producing bacteria, lowering butyrate levels and weakening the gut barrier. Local inflammation then signals the brain through neural and humoral pathways, disrupting key neurotransmitter systems such as dopamine and oxytocin. These abnormalities further aggravate gastrointestinal symptoms and contribute to behavioral changes, including decreased activity and depressive-like patterns.”

Beyond connecting stress, microbial imbalance, neural responses, and IBS symptoms into a unified framework, the study opens new paths for clinical treatment. Traditionally, patients have been treated in separate silos—gastroenterologists addressing gut symptoms while psychiatrists treat emotional issues. But as research on the brain–gut–microbiota axis advances, the concept of integrated brain–gut co-therapy is gaining momentum.

The findings suggest that restoring butyrate levels—through targeted probiotics or dietary components—may help rebalance gut ecology. At the same time, modulating neural pathways related to reward, social bonding, and emotional regulation may improve the success rate of gastrointestinal treatments. This points toward a future in which therapies target not just the gut or the brain, but the entire interconnected system.

Looking ahead, Dr. Gu hopes the research will progress from the laboratory to the clinic. “We want to move beyond treating symptoms in isolation,” she said. “Our aim is to develop comprehensive strategies that improve both emotional well-being and gastrointestinal function—making treatment more precise, more holistic, and more personalized.”

(By Michael Harper)

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Contact name: Michael Harper
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