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Depression Aggravates Immune-Mediated Hepatitis Through NLRP3 Overactivation Induced by Intestinal Microbiota.
BACKGROUND: Depression is associated with adverse effects in patients with autoimmune hepatitis (AIH). However, the underlying mechanism remains unclear. This study explores the impact of depression and related intestinal microbiota on immune-mediated hepatitis. METHODS: We assessed depression in 260 AIH patients receiving 2-year standardized treatment and 173 healthy controls. In mice, depressive-like behaviors were induced by chronic unpredictable mild stress (CUMS), and immune-mediated hepatitis was induced by intravenous injection of concanavalin A (ConA). Fecal microbiota transplantation (FMT) was performed using samples from patients with major depressive disorder (MDD) and controls. RESULTS: Depression was common in patients with AIH (106/260, 40.8%) and was associated with cirrhosis. Compared with nondepressed AIH patients, those with depression showed exacerbated intestinal barrier dysfunction and hepatic NLR family pyrin domain containing 3 (NLRP3) inflammasome overactivation. In the ConA-induced hepatitis model, CUMS exposure aggravated these abnormalities, which were then attenuated by mirtazapine. Furthermore, mice colonized with MDD microbiota exhibited greater intestinal barrier disruption and hepatic NLRP3 inflammasome overactivation than those colonized with control microbiota. Notably, gut-derived Lactococcus formosensis, isolated from the livers of MDD microbiota-colonized mice, could translocate to the liver and induce hepatic NLRP3 inflammasome overactivation. In addition, vaccination against L. formosensis prevented translocation and alleviated liver injury in monocolonized mice. CONCLUSION: Depression aggravates immune-mediated hepatitis through disruption of intestinal barrier integrity and overactivation of hepatic NLRP3 inflammasome. Gut-derived L. formosensis could translocate to the liver and induce liver injury in mice. This study provides the necessity of screening for depression in patients with AIH.
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Dysbiosis and depression: A study of gut microbiota alterations and functional pathways in antidepressant-naïve mood disorder patients.
Depression, a common mood disorder, has been associated with gut microbiota alterations, though the underlying microbial mechanisms remain unclear. This study investigated potential gut microbiota biomarkers and functional pathways in 106 antidepressant-naïve depressive patients and 151 healthy controls, with careful of confounding factors. Stool samples were analyzed using 16S rRNA sequencing, revealing significantly lower alpha diversity and distinct beta diversity in depressive patients. Eleven taxa with differential abundance were identified, including Dialister and Lactococcus (decreased) and Hungatella, Sellimonas, and Lachnoclostridium (elevated), which may relate to gut inflammation and depressive symptom severity. Functional pathway analysis highlighted 36 altered pathways, including those involved in purine degradation, lipopolysaccharide biosynthesis, and amino acid metabolism. A random forest classification model built using the identified taxa achieved moderate accuracy (~0.72) in distinguishing depressive patients from controls. Additionally, we developed a novel Depression Dysbiosis Index (DDI), which positively correlated with depression severity and effectively differentiated between groups. The DDI was robust across analyses, emphasizing its potential clinical value. Future research should incorporate longitudinal designs, advanced sequencing techniques, and additional clinical factors to deepen our understanding of the gut-brain axis in depression and improve diagnostic and therapeutic strategies.
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MicroRNA-specific targets for neuronal plasticity, neurotransmitters, neurotrophic factors, and gut microbes in the pathogenesis and therapeutics of depression.
Depression is of great concern because of the huge burden, and it is impacted by various epigenetic modifications, e.g., histone modification, covalent modifications in DNA, and silencing mechanisms of non-coding protein genes, e.g., microRNAs (miRNAs). MiRNAs are a class of endogenous non-coding RNAs. Alternations in specific miRNAs have been observed both in depressive patients and experimental animals. Also, miRNAs are highly expressed in the central nervous system and can be delivered to different tissues via tissue-specific exosomes. However, the mechanism of miRNAs' involvement in the pathological process of depression is not well understood. Therefore, we summarized and discussed the role of miRNAs in depression. Conclusively, miRNAs are involved in the pathology of depression by causing structural and functional changes in synapses, mediating neuronal regeneration, differentiation, and apoptosis, regulating the gut microbes and the expression of various neurotransmitters and BDNF, and mediating inflammatory and immune responses. Moreover, miRNAs can predict the efficacy of antidepressant medications and explain the mechanism of action of antidepressant drugs and aerobic exercise to prevent and assist in treating depression.
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Neuroimmune Advance in Depressive Disorder.
Major depressive disorder (MDD) or depression is one of the most highly prevalent, chronic, and recurrent disorders, which is associated with a high burden of disease and substantial impairment in social functions. Both immune molecules and cells have been implicated in the pathophysiology and maintenance of MDD. Findings in animals and MDD patients have suggested that both pro- and anti-inflammatory cytokines are activated in the neuroinflammation which contribute to behavioral symptoms and changes in the course of depression. There is a growing body of evidence to support that neuroinflammation is a mediator for the communication among stress response, neuroendocrine, neurotransmission, neurogenesis, and gut microbiota. These communications have been known as risk factors in the pathogenesis of MDD. In the meantime, accumulating evidence has suggested that some interventions targeting the inflammatory processes may play an important role in the treatment of MDD.
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The impact of adverse childhood experiences on gut microbiota and markers of inflammation is mediated by obesity and depression.
BACKGROUND: Adverse childhood experiences (ACEs) are associated with poor health outcomes in adulthood including obesity, psychiatric symptoms, and elevated levels of inflammatory markers. Our previous work found ACEs are associated with altered gut microbiota composition. In the present work, we examined ACE associations with gut microbiota and peripheral measures of inflammation in pregnant women with or without obesity, and explored potential modifying factors including diet and depressive symptoms. METHODS: Female participants were recruited in the third trimester of pregnancy as part of a larger growth study of African-American infants. Participants were categorized as healthy weight (BMI < 25) or obese (BMI ≥ 30) based on their early pregnancy BMI. They completed the Adverse Childhood Experiences Questionnaire (ACE-Q) and Center for Epidemiologic Studies Depression Scale (CES-D). Stool samples, blood, and dietary data were collected in the third trimester. Shotgun metagenomic sequencing was performed on DNA isolated from stool. Statistical models assessed relationships between gut microbiota and ACE. A false discovery rate (fdr) adjusted p-value q < 0.1 was considered statistically significant. RESULTS: 107 women completed questionnaires and provided stool in the third trimester. ACEs were positively associated with BMI and depressive symptom severity but not with gut microbiota composition. Depressive symptoms were significantly negatively associated with abundance of gut Bifidobacterium longum (q = 0.02) and positively associated with Bacteroides thetaiotaomicron (q = 0.02). Path analysis revealed that ACEs predicted pre-pregnancy BMI which predicted elevated inflammatory markers. ACEs also predicted more severe depressive symptoms in pregnancy, which was associated with gut microbiome composition. Finally, ACEs interacted with dietary intake of sugar and whole grains to impact markers of inflammation, the gut microbiome, and enzymes produced by gut microbiota. DISCUSSION: ACEs led to two risk pathways in pregnancy: one in which high pre-pregnancy BMI was linked with high levels of serum inflammatory markers during pregnancy, and the other in which greater depressive symptom severity was associated with alterations to the gut microbiome. Further, data suggested ACEs may influence the metabolic potential of the gut microbiome.
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Updated review of research on the gut microbiota and their relation to depression in animals and human beings.
The gut microbiota are being called the human "second brain," as they play a key role in the regulation of the central nervous system (CNS). Recent findings provide strong evidence for the presence of bidirectional communication networks between the gut microbiota and the CNS, and such crosstalk has been correlated with alterations in major depressive disorder (MDD) and other psychiatric disorders. Further, germ-free animal models have been used to investigate the effect of the microbiota on MDD and other psychiatric disorders, which have greatly expanded our knowledge of the role of the microbiota in the etiology of MDD and promoted causality studies of this psychiatric disorder and others as well. In this review, we first introduce the methodological approaches used for microbiota research and then provide an overview of current research progress on the modulatory function and composition of the gut microbiota in MDD and the therapeutic effect of probiotics that has been gained using data from human studies as well as animal experiments. Future research should focus on identification and characterization of specific bacterial strains involved in MDD with the hope of applying these findings in the prevention and treatment of MDD.
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Beneath the surface: unveiling the gut-brain axis in anorexia and depression.
Anorexia nervosa (AN) and depression are complex conditions with high comorbidity, impacting mental and physical health. Recent research suggests gut microbiota plays a significant role in their development and progression. This correspondence highlights the critical gaps in understanding the gut-brain axis in AN and depression, emphasizing the need for comprehensive research. We discuss recent findings, including altered gut microbiota profiles and inflammatory factors, and identify key areas for future investigation. These include large-scale, multi-center studies to quantify microbiota profiles, mechanistic understanding of gut microbiota alterations, and diagnostic and therapeutic advances using microbiota as biomarkers. Addressing these gaps is crucial for developing effective treatment strategies and improving patient outcomes. By exploring the underlying mechanisms, validating biomarkers, and developing targeted therapies, we can enhance diagnostic accuracy, improve treatment outcomes, and better support patients with AN and depression. This research has the potential to transform the management of these conditions and improve quality of life for those affected.Level of evidence Low level of evidence as it is a personal opinion.
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Role of Probiotics in Depression: Connecting Dots of Gut-Brain-Axis Through Hypothalamic-Pituitary Adrenal Axis and Tryptophan/Kynurenic Pathway involving Indoleamine-2,3-dioxygenase.
Depression is one of the most disabling mental disorders worldwide and characterized by symptoms including worthlessness, anhedonia, sleep, and appetite disturbances. Recently, studies have suggested that tryptophan (Trp) metabolism plays a key role in depressed mood through serotonin and kynurenine pathway involving enzyme tryptophan 5-monooxygenase (TPH) and indoleamine-2,3-dioxygenase (IDO) respectively. Moreover, during neuroinflammation, IDO is activated by proinflammatory cytokines and affects neurogenesis, cognition, disturbed hypothalamic-pituitary-adrenal (HPA) axis, and gut homeostasis by altering the gut bacteria and its metabolites like Trp derivatives. Furthermore, over the decades, researchers have focused on understanding communication between the human microbiome, especially gut microbiota, and mental health, called gut-brain-axis (GBA), particularly through Trp metabolism. Supplementation of probiotics in depression has gained attention from researchers and clinicians. However, there is limited information about probiotics supplementation on depression involving enzyme IDO and kynurenine pathway metabolites. This review discussed the potential role of probiotics in depression through the tryptophan/kynurenine pathway.
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Neural Mechanisms of Exercise: Effects on Gut Miccrobiota and Depression.
Microbiota is a set of microorganisms resident in gut ecosystem that reacts to psychological stressful stimuli, and is involved in depressed or anxious status in both animals and human being. Interestingly, a series of studies have shown the effects of physical exercise on gut microbiota dynamics, suggesting that gut microbiota regulation might act as one mediator for the effects of exercise on the brain. Recent studies found that gut microbiota dynamics are also regulated by metabolism changes, such as through physical exercise or diet change. Interestingly, physical exercise modulates different population of gut bacteria in compared to food restriction or rich diet, and alleviates gut syndromes to toxin intake. Gut microbiota could as well contribute to the beneficial effects of exercise on cognition and emotion, either directly through serotonin signaling or indirectly by modulating metabolism and exercise performance.
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Exploring the relationship between the gut microbiome and mental health outcomes in a posttraumatic stress disorder cohort relative to trauma-exposed controls.
Posttraumatic stress disorder (PTSD) imposes a significant burden on patients and communities. Although the microbiome-gut-brain axis has been proposed as a mediator or moderator of PTSD risk and persistence of symptoms, clinical data directly delineating the gut microbiome's relationship to PTSD are sparse. This study investigated associations between the gut microbiome and mental health outcomes in participants with PTSD (n = 79) and trauma-exposed controls (TECs) (n = 58). Diagnoses of PTSD, major depressive disorder (MDD), and childhood trauma were made using the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), MINI International Neuropsychiatric Interview (MINI), and Childhood Trauma Questionnaire (CTQ), respectively. Microbial communities from stool samples were profiled using 16S ribosomal RNA gene V4 amplicon sequencing and tested for associations with PTSD-related variables of interest. Random forest models identified a consortium of four genera, i.e., a combination of Mitsuokella, Odoribacter, Catenibacterium, and Olsenella, previously associated with periodontal disease, that could distinguish PTSD status with 66.4% accuracy. The relative abundance of this consortium was higher in the PTSD group and correlated positively with CAPS-5 and CTQ scores. MDD diagnosis was also associated with increased relative abundance of the Bacteroidetes phylum. Current use of psychotropics significantly impacted community composition and the relative abundances of several taxa. Early life trauma may prime the microbiome for changes in composition that facilitate a pro-inflammatory cascade and increase the risk of development of PTSD. Future studies should rigorously stratify participants into healthy controls, TECs, and PTSD (stratified by psychotropic drug use) to explore the role of the oral-gut-microbiome-brain axis in trauma-related disorders.