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Dysregulation of the gut-brain-skin axis and key overlapping inflammatory and immune mechanisms of psoriasis and depression.
The occurrence, progression and recurrence of psoriasis are thought to be related to mood and psychological disorders such as depression. Psoriasis can lead to depression, and depression, in turn, exacerbates psoriasis. No specific mechanism can explain the association between psoriasis and depression. The gut-brain-skin axis has been used to explain correlations among the gut microbiota, emotional states and systemic and skin inflammation, and this axis may be associated with overlapping mechanisms between psoriasis and depression. Therefore, in the context of the gut-brain-skin axis, we systematically summarized and comparatively analysed the inflammatory and immune mechanisms of psoriasis and depression and illustrated the dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the gut microbiota. This review provides a theoretical basis and new targets for the treatment of psoriasis and depression.
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Psychobiotics Lactiplantibacillus plantarum JYLP-326: Antidepressant-like effects on CUMS-induced depressed mouse model and alleviation of gut microbiota dysbiosis.
BACKGROUND: Depression affects a significant portion of the global population and has emerged as one of the most debilitating conditions worldwide. Recent studies have explored the relationship between depression and the microbiota of the intestine, revealing potential avenues for effective treatment. METHODS: To evaluate the potential alleviation of depression symptoms, we employed a depression C57BL/6 mice model induced by chronic unpredictable mild stress (CUMS). We administered Lactiplantibacillus plantarum JYLP-326 and conducted various animal behavior tests, including the open-field test (OFT), sucrose preference test (SPT), and tail-suspension test (TST). Additionally, we conducted immunohistochemistry staining and analyzed the hippocampal and colon parts of the mice. RESULTS: The results of the behavior tests indicated that L. plantarum JYLP-326 alleviated spontaneous behavior associated with depression. Moreover, the treatment led to significant improvements in GFAP and Iba1, suggesting its potential neuroprotective effects. Analysis of the hippocampal region indicated that L. plantarum JYLP-326 administration upregulated p-TPH2, TPH2, and 5-HT1AR, while downregulating the expression of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α. In the colon, the treatment inhibited the TLR4-MyD88-NF-κB pathway and increased the levels of occludin and ZO-1, indicating improved intestinal barrier function. Additionally, the probiotic demonstrated a regulatory effect on the HMGB1-RAGE-TLR4 signaling pathway. CONCLUSIONS: Our findings demonstrate that L. plantarum JYLP-326 exhibits significant antidepressant-like effects in mice, suggesting its potential as a therapeutic approach for depression through the modulation of gut microbiota. However, further investigations and clinical trials are required to validate its safety and efficacy for human use.
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Exploring potential causal relationships between gut microbiota, inflammatory factors, and postpartum depression: a Mendelian randomization analysis.
BACKGROUND: Recent studies have suggested a potential correlation between ecological dysregulation of the gut microbiota (GM) and the onset and development of postpartum depression (PPD). In addition, inflammatory factors (IFs) have been reported to play an important role in the development of PPD. However, the causal connections among GM, IFs, and PPD remain to be understood. OBJECTIVE: This study sought to determine if genetically predicted GM and IFs exert a causal effect on PPD and to study whether IFs mediate the causal effect of GM on PPD. METHODS: Two-step and two-sample Mendelian randomization (MR) analyses, primarily employing the inverse variance weighted (IVW) method, were conducted to evaluate the causal relationship between GM, IFs, and PPD, and to assess potential mediating effects. Heterogeneity and horizontal pleiotropy tests were performed to evaluate the robustness of the findings and the strength of the causal associations. RESULTS: Class Alphaproteobacteria, genus Family XIII AD3011 group exhibited a positive association with PPD risk; whereas, the family Clostridiales vadin BB60 group, family Veillonellaceae, genus Ruminococcaceae UCG011, and the inflammatory factors C-C motif chemokine ligand 5 (CCL5) and C-C motif chemokine ligand 3 (CCL3) demonstrated negative correlations with PPD risk. IFs did not exhibit a mediating role. No heterogeneity or horizontal pleiotropy was observed. CONCLUSIONS: Our MR study offered genetic evidence that GM and IFs contribute to the pathogenesis of PPD, with no mediating effect of IFs. This enhances our understanding of PPD's pathological mechanisms and offers new perspectives for developing novel preventative and therapeutic strategies.
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Eucommiae cortex polysaccharides attenuate gut microbiota dysbiosis and neuroinflammation in mice exposed to chronic unpredictable mild stress: Beneficial in ameliorating depressive-like behaviors.
BACKGROUND: Chronic stress alters gut microbiota composition, as well as induces inflammatory responses and behavioral deficits. Eucommiae cortex polysaccharides (EPs) have been reported to remodel gut microbiota and ameliorate obesogenic diet-induced systemic low-grade inflammation, but their role in stress-induced behavioral and physiological changes is poorly understood. METHODS: Male Institute of Cancer Research (ICR) mice were exposed to chronic unpredictable stress (CUMS) for 4 weeks and then supplemented with EPs at a dose of 400 mg/kg once per day for 2 weeks. Behavioral test-specific antidepressant and anxiolytic effects of EPs were assessed in FST, TST, EPM, and OFT. Microbiota composition and inflammation were detected using 16S ribosomal RNA (rRNA) gene sequencing, quantitative RT-PCR, western blot, and immunofluorescence. RESULTS: We found that EPs ameliorated gut dysbiosis caused by CUMS, as evidenced by increasing the abundance of Lactobacillaceae and suppressing the expansion of the Proteobacteria, thereby mitigating intestinal inflammation and barrier derangement. Importantly, EPs reduced the release of bacterial-derived lipopolysaccharides (LPS, endotoxin) and inhibited the microglia-mediated TLR4/NFκB/MAPK signaling pathway, thereby attenuating the pro-inflammatory response in the hippocampus. These contributed to restoring the rhythm of hippocampal neurogenesis and alleviating behavioral abnormalities in CUMS mice. Correlation analysis showed that the perturbed-gut microbiota was strongly correlated with behavioral abnormalities and neuroinflammation. LIMITATIONS: This study did not clarify the causal relationship between EPs remodeling the gut microbiota and improved behavior in CUMS mice. CONCLUSIONS: EPs exert ameliorative effects on CUMS-induced neuroinflammation and depression-like symptoms, which may be strongly related to their beneficial effects on gut microbial composition.
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Gut microbiota-derived indole metabolites in depression: mechanisms and therapeutic potential.
Depression, a prevalent neuropsychiatric disorder with complex pathophysiology and often insufficient treatment efficacy, is increasingly associated with disruptions in the gut-brain axis. This review focuses on the underappreciated role of the microbial indole pathway, a key route in tryptophan metabolism orchestrated by the gut microbiota. We synthesize recent evidence demonstrating that gut microbiota-derived indole metabolites, such as indole-3-propionic acid (IPA) and indole-3-aldehyde (IAld), are significantly reduced in depression. These metabolites exert multifaceted antidepressant effects by enhancing intestinal and blood-brain barrier integrity, suppressing neuroinflammation, and promoting neuroplasticity. Furthermore, we explore the therapeutic potential of targeting this axis through interventions like specific probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation to restore microbial ecology and indole metabolite levels. By highlighting the microbiota-indole-brain pathway as a critical mechanistic and therapeutic frontier, this review provides a novel perspective on the pathogenesis and treatment of depression, moving beyond conventional monoaminergic theories.
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Unraveling the Triad: A Bioinformatics Analysis of the Interplay between Prenatal Depression, Inflammation, and the Gut Microbiota.
INTRODUCTION: Prenatal depression is a prevalent mental disorder that affects women during pregnancy. Alterations in the maternal microbiota have been linked to changes in the composition of the intestinal microbiota of foetus, which can have long-term consequences for the child's health. The gut-brain axis, which involves bidirectional communication between the gut and the brain, is believed to play a role in the development of depression. METHODS: This study aimed to gather evidence for both the influence of microbiota and immunity on depression during pregnancy, using integrated bioinformatics analysis. A set of 219 differentially expressed genes (DEGs) associated with prenatal depression was established to correlate with gut inflammation. DEG data were collected from different bibliographic sources with fold change >1 and adjusted p-value <0.05. Moreover, 205 DEGs were annotated using String software. RESULTS: The protein-protein interaction networks of DEGs obtained were determined by 16 main genes: IL6, IFNG, IL1B, IL10, CD4, CXCL8, CCL2, IL2, CCL5, IL4, TGFB1, IL13, IL17A, TLR4, CRP, and BDNF. The enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways was conducted using SRplot and clusterProfiler. They were significantly involved in prenatal depression and associated with inflammation and gut microbiota. DISCUSSION: The identified genes highlight key molecular interactions between the immune system, microbiota, and brain function during pregnancy. These findings support the involvement of inflammatory and microbial pathways in the development of prenatal depression. CONCLUSION: This study identified core genes that contribute to the understanding of the molecular mechanisms involved in the development of prenatal depression, which may serve as targets for early diagnosis, prevention, and treatment.
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Glyphosate based- herbicide exposure affects gut microbiota, anxiety and depression-like behaviors in mice.
Recently, a number of studies have demonstrated the profound relationship between gut microbiota (GM) alterations and behavioral changes. Glyphosate-based herbicides (GBH) have been shown to induce behavioral impairments, and it is possible that they mediate the effects through an altered GM. In this study, we investigated the toxic effects of GBH on GM and its subsequent effects on the neurobehavioral functions in mice following acute, subchronic and chronic exposure to 250 or 500 mg/kg/day. The effect of these acute and repeated treatments was assessed at the behavioral level using the open field, the elevated plus maze, the tail suspension and splash tests. Then, mice were sacrificed and the intestinal samples were collected for GM analysis. Subchronic and chronic exposure to GBH induced an increase of anxiety and depression-like behaviors. In addition, GBH significantly altered the GM composition in terms of relative abundance and phylogenic diversity of the key microbes. Indeed, it decreased more specifically, Corynebacterium, Firmicutes, Bacteroidetes and Lactobacillus in treated mice. These data reinforce the essential link between GM and GBH toxicity in mice and suggest that observed intestinal dysbiosis could increase the prevalence of neurobehavioral alterations.
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Beneficial Effect of Alkaloids From Sophora alopecuroides L. on CUMS-Induced Depression Model Mice via Modulating Gut Microbiota.
It was recently shown that the gut microbiota of both depression patients and depression model animals is significantly altered, suggesting that gut microbes are closely related to depression. Here, we investigated the effects of Sophora alopecuroides L.-derived alkaloids on the gut microbiota of mice with depression-like behaviors. We first established a mouse model of depression via chronic unpredictable mild stress (CUMS) and detected changes in depression-like behaviors and depression-related indicators. Simultaneously, 16S rRNA sequencing was performed to investigate gut microbiota changes. Sophora alopecuroides L.-derived alkaloids improved depression-like behaviors and depression-related indicators in mice. The alkaloids decreased the gut microbiota diversity of CUMS mice and depleted intestinal differentially abundant "harmful" microbiota genera. Spearman analysis showed that there is a certain correlation between the differential microbiota (Lactobacillus, Helicobacter, Oscillospira, Odoribacter, Mucispirillum, Ruminococcus), depression-like behaviors, and depression-related indicators. Combined with the predictive analysis of gut microbiota function, these results indicate that alkaloids improve depression in mice through modulating gut microbiota.
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Oral Troxerutin Alleviates Depression Symptoms in Mice by Modulating Gut Microbiota and Microbial Metabolism.
SCOPE: A growing body of evidence suggests that the harmful gut microbiota in depression patients can play a role in the progression of depression. There is limited research on troxerutin's impact on the central nervous system (CNS), especially in depression. The study finds that troxerutin effectively alleviates depression and anxiety-like behavior in mice by increasing the abundance of beneficial bacteria like Lactobacillus and Firmicutes while decreasing the abundance of harmful bacteria like Proteobacteria, Bacteroides, and Actinobacteria in the gut. Furthermore, the research reveals that troxerutin regulates various metabolic pathways in mice, including nucleotide metabolism, caffeine metabolism, purine metabolism, arginine biosynthesis, histidine metabolism, 2-oxocarboxylic acid metabolism, biosynthesis of amino acids, glycine, serine and threonine metabolism, and Arginine and proline metabolism. CONCLUSIONS: In conclusion, the study provides compelling evidence for the antidepressant efficacy of troxerutin. Through the investigation of the role of intestinal microorganisms and metabolites, the study identifies these factors as key players in troxerutin's ability to prevent depression. Troxerutin achieves its neuroprotective effects and effectively prevents depression and anxiety by modulating the abundance of gut microbiota, including Proteobacteria, Bacteroides, and Actinobacteria, as well as regulating metabolites such as creatine.
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Gut-Brain Axis and Psychopathology: Exploring the Impact of Diet with a Focus on the Low-FODMAP Approach.
BACKGROUND: The gut-brain axis (GBA) is a bidirectional communication network connecting the central nervous system with the gastrointestinal (GI) tract, influencing both mental and physical health. Recent research has underscored the significant role of diet in modulating this axis, with attention to how specific dietary patterns can impact anxiety and depression, particularly when linked to disorders of gut-brain interaction (DGBIs), like intestinal bowel syndrome (IBS). AIMS AND METHODS: This narrative review examines the effects of specific diet regimens on the GBA and its potential role in managing psychopathology, focusing on anxiety and depression, IBS, and the low-FODMAP diet. We conducted a search on PubMed and MEDLINE by combining the following key terms: "Gut-Brain Axis", "Irritable Bowel Syndrome", "Low FODMAP diet", "Mediterranean Diet", "Psychopathology", "Anxiety and Depression", and "Gut Microbiota". We applied the following filters: "Clinical Trials", "Randomized Controlled Trials", "Reviews", "Meta-Analyses", and "Systematic Reviews". In total, 59 papers were included. RESULTS: Low-FODMAP diet, originally developed to alleviate GI symptoms in IBS, may also positively influence mental health by modulating the GBA and improving the gut microbiota (GM) composition. New insights suggest that combining the low-FODMAP diet with the Mediterranean diet could offer a synergistic effect, enhancing both GI and psychological therapeutic outcomes. CONCLUSIONS: Understanding the complex interactions between diet, the GM, and mental health opens new avenues for holistic approaches to managing psychopathology, particularly when linked to GI symptoms.