Which Gut Bacteria Is Linked to Depression? Exploring the Microbiome-Mood Connection

October 9, 2025 •

5 min read

Studies show that individuals with depression often have distinct microbial profiles compared to healthy counterparts. The emerging field of psychobiotics investigates how specific beneficial gut bacteria, as well as certain detrimental strains, are linked to depression by influencing neurotransmitters, inflammation, and stress pathways along the gut-brain axis.

Quick Summary

Scientific research has identified specific beneficial and potentially harmful gut bacteria associated with depressive symptoms, affecting mood via inflammation, neurotransmitters like serotonin and GABA, and overall gut-brain communication.

Key Points

Bacteria Associated with Depression: Certain genera, including Eggerthella, Morganella morganii, Lachnoclostridium, Hungatella, and Sellimonas, are often found in higher abundance in individuals with depressive symptoms.
Protective Bacteria: Beneficial bacteria like Lactobacillus, Bifidobacterium, Coprococcus, and Faecalibacterium are frequently depleted or less abundant in the gut of depressed individuals.
Role in Neurotransmitters: Gut bacteria influence the production of key neurotransmitters related to mood, such as serotonin, GABA, and glutamate. An imbalance can lead to disruptions in these chemical signals.
Connection to Inflammation: Dysbiosis can cause systemic inflammation and a “leaky gut,” which can negatively impact mood. Some bacteria, like Morganella morganii, are linked to promoting inflammation.
Impact on Stress Response: The gut microbiome regulates the body's stress response via the HPA axis. A healthy microbiome can foster resilience, while dysbiosis can heighten the stress response.
Promising Interventions: Modulating the gut microbiome through diet (rich in fiber and fermented foods), probiotics (containing beneficial strains), and potentially FMT shows promise as an adjunctive treatment for depression, but requires further study.
Bidirectional Communication: The connection between gut bacteria and depression is bidirectional, meaning the state of the gut can affect the brain, and mental stress can alter the gut microbiome.

The Gut-Brain Axis: A Bidirectional Link

For decades, the idea of a gut-brain connection was considered a fringe concept. However, modern science has validated and extensively studied this bidirectional communication network, referring to it as the microbiota-gut-brain axis (MGBA). This intricate highway links the central nervous system (brain) with the enteric nervous system (gut), using chemical, hormonal, and neural signaling pathways. Disruptions in this axis, known as gut dysbiosis, can have profound effects on mental health, influencing everything from mood to stress resilience. The gut microbiome, the community of microbes residing in the gastrointestinal tract, plays a pivotal role in this communication, and an imbalance has been strongly linked to the onset and progression of depressive disorders.

Specific Gut Bacteria Associated with Depression

Research has not pinpointed a single “depression-causing” bacterium but has instead identified a complex web of associations, where some bacteria are more abundant while others are depleted in individuals with depressive symptoms. A December 2022 study involving thousands of participants identified several key microbial players.

Bacteria more abundant in depressed individuals

Eggerthella: Consistently found to be more abundant in individuals with higher depressive and anxiety symptoms. A Mendelian Randomization (MR) analysis even suggests a causal link between this genus and major depressive disorder.
Morganella morganii: Linked to major depressive disorder via a mechanism involving inflammation. Research from Harvard Medical School identified a molecule produced by M. morganii that can stimulate an immune response and increase pro-inflammatory cytokines, which are associated with depression.
Lachnoclostridium: A genus belonging to the family Lachnospiraceae, studies have observed higher levels of Lachnoclostridium in individuals reporting greater depressive symptoms.
Hungatella: This genus has been associated with increased depressive symptoms and is known to produce a precursor molecule for TMAO, which has been implicated in neurological diseases, including depression.
Sellimonas: Also found to be more abundant in individuals with higher depressive symptoms, and research indicates it may be involved in inflammatory processes.

Bacteria depleted or less abundant in depressed individuals

Coprococcus: This genus of butyrate-producing bacteria is consistently found to be less abundant in individuals with depression.
Faecalibacterium: Another butyrate-producing bacterium often found in lower abundance in depressed patients. Lower levels are also associated with reduced anti-inflammatory effects.
Lactobacillus and Bifidobacterium: These well-known probiotic bacteria are frequently depleted in the gut of individuals with depression. Studies have shown that supplementation with specific strains can alleviate depressive symptoms and restore microbial balance.
Ruminococcaceae (including UCG002, UCG003, UCG005): Several genera within this family of butyrate-producing bacteria show lower abundance in those with higher depressive symptoms.
Eubacterium ventriosum: Depleted with an increase in depressive symptoms, this bacterium is also found in lower levels in animal models of traumatic brain injury, which can be linked to depression.

Mechanisms Connecting Gut Bacteria to Depression

The gut microbiome influences mental health through several interconnected mechanisms via the MGBA:

Neurotransmitter Synthesis: A large portion of the body's serotonin, a key mood-regulating neurotransmitter, is produced in the gut. Certain gut bacteria, like some strains of Lactobacillus and Eggerthella, are involved in synthesizing neuroactive substances such as serotonin, GABA, and glutamate. An imbalance can disrupt this delicate process.
Inflammation: Gut dysbiosis can increase intestinal permeability (also known as “leaky gut”), allowing inflammatory substances like lipopolysaccharides (LPS) to enter the bloodstream. This can trigger a systemic inflammatory response, which is a known contributor to depression and other chronic health issues. For example, a molecule from Morganella morganii is known to stimulate inflammatory cytokines.
Short-Chain Fatty Acids (SCFAs): Beneficial bacteria, including Coprococcus and Faecalibacterium, produce SCFAs like butyrate through the fermentation of dietary fiber. These fatty acids possess anti-inflammatory and neuroprotective properties, can cross the blood-brain barrier, and support brain function. Their depletion in depression may contribute to symptoms.
Stress Response: The gut microbiome regulates the hypothalamic-pituitary-adrenal (HPA) axis, the body's central stress response system. Dysbiosis can lead to an overactive HPA axis and increased stress hormones like cortisol, further impacting mood and mental well-being.

Comparison of Gut Bacteria Linked to Depression


Feature	Group of Bacteria (Associated with Depression)	Group of Bacteria (Associated with Resilience/Mental Well-being)
Associated Genera	Eggerthella, Morganella, Lachnoclostridium, Hungatella, Sellimonas	Coprococcus, Faecalibacterium, Lactobacillus, Bifidobacterium, Ruminococcaceae (certain UCGs)
Typical Abundance	Increased Abundance	Decreased Abundance
Neurotransmitter Impact	Potentially influence serotonin negatively; involved in glutamate metabolism.	Produce or enhance precursors for serotonin and GABA.
Influence on Inflammation	Can increase intestinal permeability and trigger systemic inflammation.	Reduce neuroinflammation and strengthen the gut barrier.
Metabolite Production	May produce precursors for inflammatory molecules or other potentially harmful metabolites.	Produce beneficial Short-Chain Fatty Acids (SCFAs) like butyrate.
Effect on Stress Response	Linked to HPA axis dysregulation and heightened stress responses.	Can help modulate the HPA axis and promote stress resilience.

Current Therapeutic and Research Directions

As the intricate link between the gut microbiome and depression becomes clearer, scientists are exploring various methods to modulate gut bacteria as a potential adjunctive therapy. These interventions include:

Psychobiotics: This term refers to live bacteria (probiotics) or substances (prebiotics) that, when ingested, produce a mental health benefit by modulating the gut-brain axis. Specific strains of Lactobacillus and Bifidobacterium are often studied for their anxiolytic and antidepressant effects.
Dietary Interventions: A diet rich in fiber, fermented foods, and healthy fats (like the Mediterranean diet) supports a diverse and healthy microbiome, which is associated with better mental health outcomes.
Fecal Microbiota Transplantation (FMT): This procedure involves transferring stool from a healthy donor to a patient. While primarily used for C. difficile infection, research shows FMT from depressed patients can induce depression-like behaviors in animal models, and FMT from healthy donors may alleviate symptoms in humans.

Conclusion

The association between specific gut bacteria and depression is a burgeoning area of research, with compelling evidence linking microbial imbalance (dysbiosis) to the pathophysiology of mood disorders. While beneficial genera like Lactobacillus, Bifidobacterium, Coprococcus, and Faecalibacterium are often found in lower abundance, potentially harmful bacteria such as Eggerthella, Morganella, and Hungatella may be elevated in individuals with depression. The complex mechanisms involve altered neurotransmitter production, systemic inflammation, and dysregulation of the stress response system. Modulating the gut microbiome through diet, psychobiotics, and other interventions holds promise as a new frontier for mental health treatment. However, the field is still maturing, and more research is needed to fully understand the causal relationships and develop effective, strain-specific therapies.

Frequently Asked Questions

Scientific evidence suggests a strong association, but it's more complex than a direct cause-and-effect relationship. Gut dysbiosis can influence inflammation, neurotransmitter production, and stress response, all of which are linked to depression. The relationship is thought to be bidirectional, where depression can also alter the microbiome.

Psychobiotics are live bacteria (probiotics) or substances (prebiotics) that, when consumed, may provide a mental health benefit by positively modulating the gut-brain axis. They may work by reducing inflammation, influencing neurotransmitter production, and regulating the body's stress response.

Studies have investigated several strains, particularly from the Lactobacillus and Bifidobacterium genera. Examples include Lactobacillus helveticus and Bifidobacterium longum, which have shown promise in reducing depressive and anxiety symptoms, especially when used alongside standard treatments.

SCFAs like butyrate are produced by beneficial gut bacteria, such as Coprococcus and Faecalibacterium, and have anti-inflammatory and neuroprotective effects. These compounds can influence brain function and are often found in lower levels in individuals with depression.

Yes, dietary changes are a primary way to modulate the gut microbiome. Diets rich in fiber and fermented foods can increase the abundance and diversity of beneficial bacteria, while a diet high in processed foods and sugar can promote harmful strains. Adopting a Mediterranean-style diet is often recommended.

Inflammation plays a key role. Gut dysbiosis can increase intestinal permeability, leading to a systemic inflammatory response. This chronic inflammation can negatively impact brain function, including mood regulation, contributing to depressive symptoms.

FMT is being explored as a potential therapy. Research has shown that FMT from depressed patients can induce depression-like behaviors in animal models. In some clinical studies, FMT has improved depressive symptoms, but more rigorous research is needed before it becomes a standard treatment for depression.