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Investigations on the Prospects of Using Lactiplantibacillus plantarum to Combat Depression through Gut Microbiota-Brain Axis.
Depression is a common neurological disorder that causes a substantial burden of disease due to higher mortality and prevalence rates. The gut microbiota plays a major role in mood regulation and offers novel insights into the etiology and management of depression. However, gut dysbiosis has a negative impact on mood, cognition, behavior, and brain development. Therefore, approaches to restore the normal gut composition, such as probiotics, prebiotics, and fecal microbiota transplant, may offer novel tactics to improve therapy for depression, among which probiotics have drawn significant attention as a therapeutic intervention. Although there is no consensus on the most effective probiotic strain for treating depression, Lactiplantibacillus plantarum (L. plantarum) has gained considerable prominence due to its therapeutic potential in managing depression. The mechanisms by which L. plantarum regulates depression involve modulating the gut-brain axis through the production of various compounds, including gamma-aminobutyric acid (GABA), tryptophan, lactate, short-chain fatty acids (SCFAs), acetylcholine, and vitamins. This review highlights the antidepressant potential of L. plantarum through modulation of the gut microbiota and explores the possible mechanism of action of L. plantarum and its metabolites, as well as the genetic and epigenetic regulation of host responses and potential microRNA interactions that modulate the gut microbiota. Furthermore, metabolic engineering techniques for the L. plantarum strain, as well as promising strategies for delivering L. plantarum to the brain, have been discussed. A deeper insight into the mechanisms and gut microbiota interventions may provide effective treatment approaches for depression.
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The Immune Mind: Linking Dietary Patterns, Microbiota, and Psychological Health.
Background/Objectives: Nutritional patterns influence the gut-brain axis and immune signaling with potential consequences for depression and anxiety. We conducted a review focused on clinically meaningful psychiatric outcomes (symptom severity/diagnosis) to synthesize recent evidence (2020-2025) on Mediterranean-style dietary interventions; ultra-processed food (UPF) exposure; and psychobiotic/prebiotic strategies, integrating mechanistic insights relevant to practice. Methods: Searches in PubMed/MEDLINE, Scopus, and Web of Science (January 2020-October 2025) combined terms for diet, Mediterranean diet (MD), UPF, microbiota, probiotics, psychobiotics, depression, and anxiety. Eligible designs were randomized/controlled trials (RCTs), prospective cohorts, and systematic reviews/meta-analyses reporting clinical psychiatric outcomes in adults. We prioritized high-quality quantitative syntheses and recent RCTs; data were extracted into a prespecified matrix and synthesized narratively. Results: Recent systematic reviews/meta-analyses support that MD interventions reduce depressive symptoms in adults with major or subthreshold depression, although large, long-term, multicenter RCTs remain a gap. Exposure to UPF is consistently associated with higher risk of common mental disorders and depressive outcomes in large prospective cohorts. Psychobiotics (specific probiotic strains and prebiotics) show small-to-moderate benefits on depressive symptoms across clinical and nonclinical samples, with heterogeneity in strains, dosing, and duration. Mechanistic reviews implicate microbiota-derived metabolites (short-chain fatty acids) and immune-inflammatory signaling (including tryptophan-kynurenine pathways) as plausible mediators. Conclusions: Clinically, emphasizing Mediterranean-style dietary patterns, reducing UPF intake, and considering targeted psychobiotics may complement standard psychiatric care for depression. Future work should prioritize adequately powered, longer RCTs with standardized dietary protocols and microbiome-informed stratification to clarify responders and mechanisms.
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[Potential biological mechanisms underlying spaceflight-induced depression symptoms in astronauts].
Long-term spaceflight exposes astronauts to multiple extreme environmental factors, such as cosmic radiation, microgravity, social isolation, and circadian rhythm disruption, that markedly increase the risk of depressive symptoms, posing a direct threat to mental health and mission safety. However, the underlying biological mechanisms remain complex and incompletely understood. The potential mechanisms of spaceflight-induced depressive symptoms involve multiple domains, including alterations in brain structure and function, dysregulation of neurotransmitters and neurotrophic factors, oxidative stress, neuroinflammation, neuroendocrine system imbalance, and gut microbiota disturbances. Collectively, these changes may constitute the biological foundation of depressive in astronauts during spaceflight. Space-related stressors may increase the risk of depressive symptoms through several pathways: impairing hippocampal neuroplasticity, suppressing dopaminergic and serotonergic system function, reducing neurotrophic factor expression, triggering oxidative stress and inflammatory responses, activating the hypothalamic-pituitary-adrenal axis, and disrupting gut microbiota homeostasis. Future research should integrate advanced technologies such as brain-computer interfaces to develop individualized monitoring and intervention strategies, enabling real-time detection and effective prevention of depressive symptoms to safeguard astronauts' psychological well-being and mission safety.
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Fecal Short-Chain Fatty Acid Ratios as Related to Gastrointestinal and Depressive Symptoms in Young Adults.
OBJECTIVE: Short-chain fatty acids (SCFAs) are produced by the gut microbiota and may reflect health. Gut symptoms are common in individuals with depressive disorders, and recent data indicate relationships between gut microbiota and psychiatric health. We aimed to investigate potential associations between SCFAs and self-reported depressive and gut symptoms in young adults. METHODS: Fecal samples from 164 individuals (125 were patients with psychiatric disorders: mean [standard deviation] age = 21.9 [2.6] years, 14% men; 39 nonpsychiatric controls: age = 28.5 [9.5] years, 38% men) were analyzed for the SCFA acetate, butyrate, and propionate by nuclear magnetic resonance spectroscopy. We then compared SCFA ratios with dimensional measures of self-reported depressive and gut symptoms. RESULTS: Depressive symptoms showed a positive association with acetate levels (ρ = 0.235, p = .003) and negative associations with both butyrate (ρ = -0.195, p = .014) and propionate levels (ρ = -0.201, p = .009) in relation to total SCFA levels. Furthermore, symptoms of diarrhea showed positive associations with acetate (ρ = 0.217, p = .010) and negative associations with propionate in relation to total SCFA levels (ρ = 0.229, p = 0-007). Cluster analysis revealed a heterogeneous pattern where shifts in SCFA ratios were observed in individuals with elevated levels of depressive symptoms, elevated levels of gut symptoms, or both. CONCLUSIONS: Shifts in SCFAs are associated with both depressive symptoms and gut symptoms in young adults and may have of relevance for treatment.
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Oral microbiota dysbiosis alters chronic restraint stress-induced depression-like behaviors by modulating host metabolism.
Studies have shown that the microbiota-gut-brain axis is highly correlated with the pathogenesis of depression in humans. However, whether independent oral microbiome that do not depend on gut microbes could affect the progression of depression in human beings remains unclear, neither does the presence and underlying mechanisms of the microbiota-oral-brain axis in the development of the condition. Hence this study that encompasses clinical and animal experiments aims at investigating the correlation between oral microbiota and the onset of depression via mediating the microbiota-oral-brain axis. We compared the oral microbial compositions and metabolomes of 87 patients with depressive symptoms versus 70 healthy controls. We found that the oral microbial and metabolic signatures were significantly different between the two groups. Significantly, germ-free (GF) mice transplanted with saliva from mice exposing to chronic restraint stress (CRS) displayed depression-like behavior and oral microbial dysbiosis. This was characterized by a significant differential abundance of bacterial species, including the enrichment of Pseudomonas, Pasteurellaceae, and Muribacter, as well as the depletion of Streptococcus. Metabolomic analysis showed the alternation of metabolites in the plasma of CRS-exposed GF mice, especially Eicosapentaenoic Acid. Furthermore, oral and gut barrier dysfunction caused by CRS-induced oral microbiota dysbiosis may be associated with increased blood-brain barrier permeability. Pseudomonas aeruginosa supplementation exacerbated depression-like behavior, while Eicosapentaenoic Acid treatment conferred protection against depression-like states in mice. These results suggest that oral microbiome and metabolic function dysbiosis may be relevant to the pathogenesis and pathophysiology of depression. The proposed microbiota-oral-brain axis provides a new way and targets for us to study the pathogenesis of depression.
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Antidepressant effect of carvedilol on streptozotocin-induced diabetic peripheral neuropathy mice by altering gut microbiota.
RATIONALE: Although diabetic peripheral neuropathic pain (DPNP) and depression have been recognized for many years, their co-morbidity relationship and effective treatment choices remain uncertain. OBJECTIVES: To evaluate the antidepressant effect of carvedilol on streptozotocin-induced DPNP mice, and the relationship with gut microbiota. METHODS: The hyperalgesia and depressive behaviors of mice with comorbidity of DPNP and depression were confirmed by pain threshold of the mechanical sensitivity test (MST), immobility time of the tail suspension test (TST) and the forced swimming test (FST). The anti-depressive effect and fecal gut microbiota composition were studied in DPNP mice treated with carvedilol (10 mg/kg/day), and the relationships between them were analyzed by Spearman's correlation. RESULTS: Depression was successfully induced in DPNP mice. Carvedilol can reverse the decreased mechanical pain threshold and relieve the depressive behaviors of DPNP mice, while increasing the abundance of Prevotella, Ruminococcus, Helicobacter and Desulfovibrio, and decreasing the abundance of Akkermansia and Allobaculum. CONCLUSIONS: Carvedilol can alleviate the mechanical hyperalgesia and alter gut microbiota to ameliorate the depression-like behaviors which induced by DPNP.
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The Potential Mediating Role of Depressive Symptoms in the Inverse Association Between Dietary Index of Gut Microbiota and Overactive Bladder: A Cross-Sectional Study.
Overactive bladder (OAB) is a prevalent urinary dysfunction with a substantial burden. Diet, gut microbiota, and psychological factors such as depression are increasingly implicated in disease pathways, yet evidence from large-scale studies remains limited. This study investigates the association between the dietary index of gut microbiota (DI-GM) and OAB using weighted regression and examines whether depressive symptoms serve as a potential mediator through mediation analysis. Data from 30 014 adults in the 2007-2020 National Health and Nutrition Examination Survey (NHANES) were analyzed. DI-GM scores were derived from dietary recalls; OAB was defined by standardized symptom criteria; depressive symptoms were measured using the Patient Health Questionnaire-9 (PHQ-9). Logistic regression, sensitivity, and mediation effect analysis were conducted. Among participants, 6320 had OAB (weighted prevalence 21.0%). Higher DI-GM scores were associated with lower odds of OAB (fully adjusted odds ratio [OR] = 0.956, p < 0.001), mainly driven by beneficial dietary components. Depressive symptoms mediated 25.8% of the association, rising to 35.4% for beneficial components. A gut microbiota-supportive dietary pattern is inversely associated with OAB prevalence, underscoring the importance of diet quality in bladder health. Depressive symptoms potentially mediated this link, suggesting dietary interventions may be complemented by psychological support.
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Ghrelin in Depression: A Promising Therapeutic Target.
Depression is a widespread disease affecting over 300 million individuals of various ethnicities and socioeconomic backgrounds globally. It frequently strikes early in life and becomes a chronic or recurring lifelong illness. Out of the various hypotheses for the pathophysiology of depression, the gut-brain axis and stress hypothesis are the ones that need to be researched, as psychological stress impairs one or more pathways of the brain-gut axis and is likely to cause brain-gut axis dysfunction and depression. A dysfunctional reciprocal gut-brain relationship may contribute to many diseases, including inflammatory disorders, abnormal stress responses, impaired behavior, and metabolic changes. The hormone ghrelin is a topic of interest concerning the gut-brain axis as it interacts with the gut-brain axis indirectly via the central nervous system or via crossing the blood-brain barrier. Ghrelin release is also affected by the gut microbes, which has also been discussed in the review. This review elaborates on Ghrelin's role in depression and its effect on various aspects like neurogenesis, HPA axis, and neuroinflammation. Furthermore, this review focuses on ghrelin as a potential target for alleviation of depressive symptoms.
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A Pilot Study of the Gut Microbiota Associated With Depressive Symptoms and Sleep Disturbance Among Chinese and Korean Immigrants in the United States.
CONTEXT: Depression is prevalent among Asian Americans (AsA) during the COVID-19 pandemic, and depression often leads to sleep disturbance in this population. The gut microbiota (GM) plays a critical role in mental health and sleep quality, and the composition of the GM is largely unknown among AsA. OBJECTIVES: Examine associations of the GM with depressive symptoms and sleep disturbance among Chinese and Korean American immigrants. METHODS: Depressive symptoms (PROMIS Short Form-Depression) and sleep quality (Pittsburgh Sleep Quality Index [PSQI]) were collected via surveys. PROMIS measure T-score > 55 indicates positive depressive symptoms, and a total PSQI score > 5 indicates sleep disturbance. 16S rRNA V3-V4 gene regions were sequenced from fecal specimens to measure GM. Permutational multivariate analysis of variance and linear discriminant analysis effect size were applied to examine associations of the GM with symptoms. RESULTS: Among 20 participants, 55% (n = 11) reported depressive symptoms and 35% (n = 7) reported sleep disturbance. A higher α-diversity was marginally associated with lower depressive symptoms: Chao1 (r = -0.39, p = 0.09) and Shannon index (r = -0.41, p = 0.08); β-diversity distinguished participants between categories of depressive symptoms (weighted UniFrac, p=0.04) or sleep disturbance (Jaccard, p=0.05). Those with depressive symptoms showed a higher abundance of Actinobacteria, while those without depressive symptoms had a higher abundance of Bacteroidetes. No significant taxa were identified for sleep disturbance. CONCLUSIONS: Gut microbial diversity showed promising associations with depressive symptoms and sleep disturbance among Chinese and Korean immigrants. Specific taxa were identified as associated with depressive symptoms. Future studies with a larger sample size are warranted to confirm our findings.
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Fecal microbiota composition and function are associated with anxiety and depression in patients with inflammatory bowel disease.
BACKGROUND AND AIMS: Increasing prevalence of anxiety and depression are found in patients with inflammatory bowel disease (IBD). Altered gut microbiome may affect the brain, resulting in psychiatric symptoms. We aimed to analyze the feature of gut microbiota in IBD patients with anxiety or depression. METHODS: Anxiety and depression symptoms were assessed by the Hospital Anxiety and Depression Scale (HADS). Stool samples were collected from IBD patients, and the 16S rRNA sequencing was used to detect fecal microbiota. Metabolites were detected by Liquid Chromatography-Mass Spectrometry (LC-MS). RESULTS: Among the involved IBD patients (n = 59), 28.81% had anxiety and 33.90% had depression. Linear discriminant analysis Effect Size (LEfSe) (LDA > 3.0) revealed that 4 genera (Klebsiella, Alloprevotella, Barnesiella, Bacillus) were enriched, while Sellimonas was depleted in the anxiety group. Enrichment of 2 genera (Ruminococcus, Barnesiella) were found in the depression group. In the anxiety group, valine, leucine and isoleucine degradation was enriched in fecal microbiota, with upregulation of 3-methyl-2-oxobutanoic acid involved in the above pathway. In the depression group, butanoate metabolism was enriched in fecal microbiota, with alpha-ketoglutaric acid involved. Lysine degradation were enriched in fecal microbiota, with pipecolic acid involved. Primary bile acid biosynthesis was depleted in fecal microbiota, with glycocholic acid involved. Pearson correlation analysis revealed a positive correlation between Alloprevotella and 3-methyl-2-oxobutanoic acid in the anxiety group. In patients with both anxiety and depression, four genera (Subdoligranulum, Alloprevotella, Christensenellaceae R-7 group, Barnesiella) were positively correlated with alpha-ketoglutaric acid. CONCLUSION: In this study, the alteration of composition of fecal microbiota was identified, and differential genus associated with IBD patients with anxiety or depression or both were explored. Change in function of microbiota was also discovered by the detection of differential pathways and fecal metabolites, which were associated with IBD patients with anxiety or depression or both.