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Bifidobacterium infantis M-63 improves mental health in victims with irritable bowel syndrome developed after a major flood disaster.
Individuals in a community who developed irritable bowel syndrome (IBS) after major floods have significant mental health impairment. We aimed to determine if Bifidobacterium infantis M-63 was effective in improving symptoms, psychology and quality of life measures in flood-affected individuals with IBS and if the improvement was mediated by gut microbiota changes. Design was non-randomised, open-label, controlled before-and-after. Of 53 participants, 20 with IBS were given B. infantis M-63 (1×109 cfu/sachet/day) for three months and 33 were controls. IBS symptom severity scale, hospital anxiety and depression scale, SF-36 Questionnaire, hydrogen breath testing for small intestinal bacterial overgrowth and stools for 16S rRNA metagenomic analysis were performed before and after intervention. 11 of 20 who were given probiotics (M-63) and 20 of 33 controls completed study as per-protocol. Mental well-being was improved with M-63 vs controls for full analysis (P=0.03) and per-protocol (P=0.01) populations. Within-group differences were observed for anxiety and bodily pain (both P=0.04) in the M-63 per-protocol population. Lower ratio of Firmicutes/Bacteroidetes was observed with M-63 vs controls (P=0.01) and the lower ratio was correlated with higher post-intervention mental score (P=0.04). B. infantis M-63 is probably effective in improving mental health of victims who developed IBS after floods and this is maybe due to restoration of microbial balance and the gut-brain axis. However, our conclusion must be interpreted within the context of limited sample size. The study was retrospectively registered on 12 October 2017 and the Trial Registration Number (TRN) was NCT03318614.
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Gut dysbiosis induces the development of depression-like behavior through abnormal synapse pruning in microglia-mediated by complement C3.
BACKGROUND: Remodeling eubiosis of the gut microenvironment may contribute to preventing the occurrence and development of depression. Mounting experimental evidence has shown that complement C3 signaling is associated with the pathogenesis of depression, and disruption of the gut microbiota may be an underlying cause of complement system activation. However, the mechanism by which complement C3 participates in gut-brain crosstalk in the pathogenesis of depression remains unknown. RESULTS: In the present study, we found that chronic unpredictable mild stress (CUMS)-induced mice exhibited obvious depression-like behavior as well as cognitive impairment, which was associated with significant gut dysbiosis, especially enrichment of Proteobacteria and elevation of microbiota-derived lipopolysaccharides (LPS). In addition, peripheral and central complement C3 activation and central C3/CR3-mediated aberrant synaptic pruning in microglia have also been observed. Transplantation of gut microbiota from CUMS-induced depression model mice into specific pathogen-free and germ-free mice induced depression-like behavior and concomitant cognitive impairment in the recipient mice, accompanied by increased activation of the complement C3/CR3 pathway in the prefrontal cortex and abnormalities in microglia-mediated synaptic pruning. Conversely, antidepressants and fecal microbiota transplantation from antidepressant-treated donors improved depression-like behaviors and restored gut microbiome disturbances in depressed mice. Concurrently, inhibition of the complement C3/CR3 pathway, amelioration of abnormal microglia-mediated synaptic pruning, and increased expression of the synapsin and postsynaptic density protein 95 were observed. Collectively, our results revealed that gut dysbiosis induces the development of depression-like behaviors through abnormal synapse pruning in microglia-mediated by complement C3, and the inhibition of abnormal synaptic pruning is the key to targeting microbes to treat depression. CONCLUSIONS: Our findings provide novel insights into the involvement of complement C3/CR3 signaling and aberrant synaptic pruning of chemotactic microglia in gut-brain crosstalk in the pathogenesis of depression. Video Abstract.
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Prophylactic effect of Tongxieyaofang polysaccharide on depressive behavior in adolescent male mice with chronic unpredictable stress through the microbiome-gut-brain axis.
Major depression disorder is more common among adolescents and is a primary reason for suicide in adolescents. Some antidepressants are ineffective and may possess side effects. Therefore, developing an adolescent antidepressant is the need of the hour. We designed the stress model of adolescent male mice induced by chronic unpredictable stress (CUS). The mice were treated using Tongxieyaofang neutral polysaccharide (TXYF-NP), Tongxieyaofang acidic polysaccharide (TXYF-AP), TXYF-AP + TXYF-NP and fructooligosaccharide + galactooligosaccharides to determine their body weight, behavior, and serum hormone levels. RT-qPCR was used to detect the gene expression of Crhr1, Nr3c1, and Nr3c2 in the hypothalamus and hippocampus and the gene expression of glutamic acid and γ-aminobutyric acid-related receptors in the hippocampus. RT-qPCR, Western blot, and ELISA detected tryptophan metabolism in the colon, serum, and hippocampus. 16s rDNA helped sequence colon microflora, and non-targeted metabolomics enabled the collection of metabolic profiles of colon microflora. In adolescent male mice, CUS induced depression-like behavior, hypothalamic-pituitary-adrenal axis hyperactivity, hippocampal tissue damage, abnormal expression of its related receptors, and dysregulation of tryptophan metabolism. The 16s rDNA and non-targeted metabolomics revealed that CUS led to colon microflora disorder and bile acid metabolism abnormality. Tongxieyaofang polysaccharide could improve the bacterial community and bile acid metabolism disorder by upregulating the relative abundance of Lactobacillus gasseri, Lachnospiraceae bacterium 28-4, Bacteroides and Ruminococcaceae UCG-014 while preventing CUS-induced changes. TXYF-P can inhibit depression-like behavior due to CUS by regulating colonic microflora and restoring bile acid metabolism disorder. Thus, based on the different comparisons, TXYF-NP possessed the best effect.
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Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease.
BACKGROUND: Many inflammatory bowel disease (IBD) patients follow a restrictive diet due to perceived positive effects on their symptoms. We assessed the prevalence of vegetarian (VD) and gluten-free diets (GFDs) in IBD patients, the reasons for following such a diet, and whether nutrition has an impact on disease activity and microbiota composition. METHODS: We included 1254 patients from the Swiss Inflammatory Bowel Disease Cohort Study with prospective acquisition of clinical data and psychosocial, disease-related and lifestyle factors between 2006 and 2015. Dietary habits were assessed through a self-report questionnaire. In 92 patients, we analysed intestinal mucosa-associated microbial composition using high-throughput sequencing. RESULTS: Overall, 4.1% (n = 52) of the patients reported following a VD and 4.7% (n = 54) a GFD. No differences regarding disease activity, fistula, hospitalization or surgery rates were observed. Patients on a VD or GFD had significantly higher levels of post-traumatic stress symptoms. Furthermore, GFD patients had significantly higher anxiety and depression symptom levels. The gut microbiota composition in IBD patients following a VD or GFD was significantly different compared to that of omnivores. CONCLUSIONS: Although we did not identify a relevant impact of a specific diet on the course of the disease, there was a significant association with lower psychological well-being in VD and GFD patients.
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The function of the gut microbiota-bile acid-TGR5 axis in diarrhea-predominant irritable bowel syndrome.
UNLABELLED: Imbalanced gut microbiota (GM) and abnormal fecal bile acid (BA) are thought to be the key factors for diarrhea-predominant irritable bowel syndrome (IBS-D), but the underlying mechanism remains unclear. Herein, we explore the influence of the GM-BA-Takeda G-protein-coupled receptor 5 (TGR5) axis on IBS-D. Twenty-five IBS-D patients and fifteen healthy controls were recruited to perform BA-related metabolic and metagenomic analyses. Further, the microbiota-humanized IBS-D rat model was established by fecal microbial transplantation (FMT) to investigate the GM-BA-TGR5 axis effects on the colonic barrier and visceral hypersensitivity (VH) in IBS-D. Finally, we used chenodeoxycholic acid (CDCA), an important BA screened out by metabolome, to evaluate whether it affected diarrhea and VH via the TGR5 pathway. Clinical research showed that GM associated with bile salt hydrolase (BSH) activity such as Bacteroides ovatus was markedly reduced in the GM of IBS-D, accompanied by elevated total and primary BA levels. Moreover, we found that CDCA not only was increased as the most important primary BA in IBS-D patients but also could induce VH through upregulating TGR5 in the colon and ileum of normal rats. TGR5 inhibitor could reverse the phenotype, depression-like behaviors, pathological change, and level of fecal BSH in a microbiota-humanized IBS-D rat model. Our findings proved that human-associated FMT could successfully induce the IBS-D rat model, and the imbalanced GM-BA-TGR5 axis may promote colonic mucosal barrier dysfunction and enhance VH in IBS-D. IMPORTANCE: Visceral hypersensitivity and intestinal mucosal barrier damage are important factors that cause abnormal brain-gut interaction in diarrhea-predominant irritable bowel syndrome (IBS-D). Recently, it was found that the imbalance of the gut microbiota-bile acid axis is closely related to them. Therefore, understanding the structure and function of the gut microbiota and bile acids and the underlying mechanisms by which they shape visceral hypersensitivity and mucosal barrier damage in IBS-D is critical. An examination of intestinal feces from IBS-D patients revealed that alterations in gut microbiota and bile acid metabolism underlie IBS-D and symptom onset. We also expanded beyond existing knowledge of well-studied gut microbiota and bile acid and found that Bacteroides ovatus and chenodeoxycholic acid may be potential bacteria and bile acid involved in the pathogenesis of IBS-D. Moreover, our data integration reveals the influence of the microbiota-bile acid-TGR5 axis on barrier function and visceral hypersensitivity.
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Chimonanthus nitens Oliv. Leaf Granule Ameliorates DSS-Induced Acute Colitis Through Treg Cell Improvement, Oxidative Stress Reduction, and Gut Microflora Modulation.
The rising incidence of ulcerative colitis has become a new challenge for public health. Chimonanthus nitens Oliv. leaf granule (COG) is a natural medicine used for the treatment of respiratory diseases, which has excellent anti-inflammatory and antioxidant effects. However, the therapeutic effect of COG in ulcerative colitis (UC) has not been reported. Here, the experimental colitis was treated with dextran sodium sulfate (DSS) and COG. After treatment with high (30 g/kg), medium (15 g/kg), and low (7.5 g/kg) doses of COG for 11 consecutive days, the body weight, disease activity index (DAI) score, colon length, colon weight index, and the pathological score of mice were effectively improved. COG significantly reduced the levels of inflammatory cytokines in UC mice in vitro and in vivo and restored the secretion levels of IL-6 and IL-10 in the colon. Meanwhile, compared to mice with colitis, COG-treated mice showed lower levels of MDA, MPO, NO, and eNOS and higher levels of GSH-Px and MAO, which indicated that oxidative stress damage in colitic mice was alleviated by COG. Moreover, less Th17 and more Tregs were observed in the COG-treated groups. In addition, COG improved the diversity and relative abundance of gut microflora in the colon of colitic mice, and Lachnospiraceae_NK4A136_group and Lachnospiraceae_UCG-006 were obviously regulated at the genus level. In summary, COG has a protective effect on DSS-induced experimental colitis, mainly through inhibition of immune-inflammatory responses and oxidative stress and regulation of mTreg cell responses and intestinal flora composition.
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Acute sleep deprivation exacerbates systemic inflammation and psychiatry disorders through gut microbiota dysbiosis and disruption of circadian rhythms.
Acute sleep deprivation (ASD) is often observed in shift workers and characterized by drowsiness and unrelenting exhaustion. The physiological and psychological effects of ASD include anxiety, depression, cognitive impairment, systemic inflammation, stress responses, and disruptions of gut microbiota. However, the mechanisms involved in the ASD-associated circadian dysregulations with regard to gut dysbiosis, systemic inflammation, physiological modulation, and psychiatry disorders remain unclear. The aim of this study was to investigate whether central nervous system disorders induced by ASD are related to inflammation, barrier dysfunction, and circadian dysregulation. We also assessed impacts on microbiota succession. Male C57BL/6 mice were randomly allocated to the control and sleep deprivation (SD) groups. Mice in the SD group were subjected to 72 h of paradoxical SD using the modified multiple-platform method for ASD induction (72 h rapid eye movement-SD). The effects of ASD on dietary consumption, behaviors, cytokines, microbiota, and functional genes were determined. The appetite of the SD group was significantly higher than that of the control group, but the body weight was significantly lower than that of the control group. The anxiety-like behaviors were found in the SD group. Alpha and beta diversity of microbiota showed significant decrease after ASD induction; the relative abundance of Candidatus_Arthromitus and Enterobacter was increased, whereas that abundance of Lactobacillus, Muribaculum, Monoglobus, Parasutterella, and others was decreased in the SD group. These effects were accompanied by reduction in fecal propionic acid. In the proximal colon, the SD group exhibited significantly higher inflammation (tumor necrosis factor-α [TNF-α]) and dysregulation of the circadian rhythms (brain and muscle ARNT-like 1 [BMAL1] and cryptochrome circadian regulator 1 [CRY1]) and tight junction genes (occludin [OCLN]) than the control group. Gut barrier dysfunction slightly increased the plasma concentration of lipopolysaccharide and significantly elevated TNF-α. Inflammatory signals might be transduced through the brain via TNF receptor superfamily member 1 A (TNFRSF1A), which significantly increased the levels of microglia activation marker (ionized calcium-binding adapter molecule 1 [IBA1]) and chemokine (intercellular adhesion molecule 1 [ICAM1]) in the cerebral cortex. The serotonin receptor (5-hydroxytryptamine 1A receptor [5-HT1AR]) was significantly downregulated in the hippocampus. In summary, 72 h of rapid eye movement-SD induced physiological and psychological stress, which led to disruption of the circadian rhythms and gut microbiota dysbiosis; these effects were related to decrement of short chain fatty acids, gut inflammation, and hyperpermeability. The microbiota may be utilized as preventive and therapeutic strategies for ASD from the perspectives of medicine and nutrition.
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Fecal metabolites as early-phase biomarkers and prediction panel for ischemic stroke.
BACKGROUND: There is growing research on the relationship between gut bacteria and various forms of strokes. This study aimed to investigate the relationship between fecal metabolites and ischemic stroke, providing a new perspective on predicting the latter. RESULTS: Stool samples were taken from 60 patients with ischemic stroke and 60 healthy individuals, and non-targeted metabolomic analysis was used. The generalized boosted linear model was utilized for co-occurrence analysis to ascertain the noteworthy variation in fecal metabolites. The important differential metabolites were identified by the random forest algorithm, a prediction panel was developed to distinguish ischemic stroke patients from healthy individuals. Specifically, six differential metabolites (Ganoderic acid theta, Fructose-lysine, Pentaethylene glycol, 2-Chlorooctadecanoic acid, PA(2:0/PGF1alpha), and 4-[(E)-5,6-Dihydro-2,3'-bipyridin-3(4H)-ylidenemethyl]-3-methoxyphenol) were identified as potential independent stroke-associated metabolites. A prediction panel consisting of these six metabolites could yield an area under the curve of 0.989 in training set and 0.973 in testing set. There was a substantial correlation between all six independent stroke-associated metabolites and the severity of ischemic stroke, but it was not affected by depression or anxiety. CONCLUSIONS: These six differential metabolites were independent stroke-associated metabolites, and the panel consisting of these metabolites could serve as a potential prediction panel for ischemic stroke. However, future external validation in multi-ethnic cohorts is necessary to confirm broader generalizability.
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[Clinical study on efficacy and mechanism of separated moxibustion in the treatment of rheumatoid arthritis and related negative emotions based on gut microbiota].
OBJECTIVES: To investigate the clinical efficacy of separated moxibustion in the treatment of rheumatoid arthritis (RA) and related negative emotions based on gut microbiota, so as to explore its potential mechanism of action. METHODS: A total of 70 RA patients were randomly divided into a control group (n=35, 2 cases dropped off, 3 cases were excluded) and an observation group (n=35, 3 cases dropped off, 2 cases were excluded), and 30 healthy participants who underwent physical examination during the same period were randomly enrolled as the normal group. The control group was given conventional drug therapy;the observation group was additionally treated with separated moxibustion at bilateral Zusanli (ST36), Shenshu (BL23) and Ashi points on the basis of the control group, once every other day, 3 times a week, for 5 consecutive weeks. The scores of disease activity score in 28 joints (DAS28), visual analogue scale (VAS) for pain, morning stiffness, gastrointestinal symptom rating scale (GSRS), self-rating anxiety scale (SAS), and self-rating depression scale (SDS) were compared between the control group and observation group before and after treatment. 16S ribosomal RNA (rRNA) gene sequencing was used to detect the composition structure and relative abundance of gut microbiota in the 3 groups before and after treatment. ELISA was adopted to measure the serum contents of lipopolysaccharide (LPS), lipopolysaccharide-binding protein (LBP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), 5-hydroxytryptamine (5-HT), and insulin-like growth factor-1 (IGF-1) in the control and observation groups before and after treatment. RESULTS: Compared with the baseline in the same group, the scores of DAS28, VAS, GSRS, SAS, SDS, as well as serum contents of LPS, LBP, TNF-α, IL-1β and IL-6 were significantly decreased in both the control and observation groups after treatment (P<0.05, P<0.01), and the reductions in the observation group were more significant than those in the control group (P<0.05, P<0.01). In contrast, morning stiffness score was significantly decreased, and serum contents of 5-HT and IGF-1 were significantly increased in the observation group after treatment compared with baseline and those in the control group after treatment (P<0.05, P<0.01). Before treatment, compared with the normal group at the same time point, the α -diversity of gut microbiota (Chao1, Ace, Sobs, Shannon indices) and the abundances of beneficial bacteria (Bacteroidota, Faecalibacterium, Bacteroides, Bifidobacterium) in the observation and control groups were significantly lower (P<0.01), while the Firmicutes/Bacteroidota (F/B) ratio and the abundances of opportunistic pathogenic bacteria (Firmicutes, Prevotella, Proteobacteria, Actinobacteriota, Escherichia-Shigella, Klebsiella) were significantly higher (P<0.01). Microbiota clustering analysis showed significant differences between the observation/control groups and the normal group. After treatment, all the above indicators were improved in observation/control groups, and the observation group showed significantly better outcomes in increasing α -diversity, restoring beneficial bacteria abundance, and reducing F/B ratio and pathogenic bacteria abundance than the control group (P<0.01, P<0.05). CONCLUSIONS: Separated moxibustion combined with conventional drugs exerts superior clinical efficacy to monotherapy with conventional drugs in relieving joint pain, improving gastrointestinal symptoms, and alleviating anxiety and depression in RA patients. Its mechanism may be associated with regulating gut microbiota diversity, optimizing microbiota structure, reducing inflammatory factor levels, and improving neurotransmitter metabolism.
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The probiotic Lactobacillus kefiranofaciens K6 alleviates exercise and sleep deprivation-induced physiological dysregulation and neuropsychiatric disorders via modulation of inflammation, circadian rhythm, and stress response.
Individuals often suffer from insufficient or disrupted sleep due to night shifts, work pressure, and irregular lifestyles. Sleep deprivation (SD), defined as an intentional or unintentional reduction in sleep quality or quantity, has been associated with an increased risk of metabolic disorders, gut dysbiosis, emotional disturbances, and diminished performance in occupational and physical activities. Functional probiotics have been shown to regulate physiological homeostasis and ameliorate diseases through their impact on the microbiota and various physiological pathways. In this study, we employed the modified multiple platform method (MMPM) to induce SD in an animal model, simulating physiological dysregulation and psychological characteristics associated with SD. We further investigated whether exercise and the probiotic Lactobacillus kefiranofaciens K6 could mitigate the effects of SD on physiological homeostasis, neuropsychological function, inflammation, circadian rhythm, and exercise capacity. We found that the probiotic K6 significantly alleviated depression and anxiety while improving glucose intolerance and declining endurance capacity in the SD model. Elevated injury indexes (CK and LDH) induced by SD combined with exercise training were also significantly reduced under K6 supplementation. In the liver and muscle, SD alone or combined with exercise led to inflammation (TNF-α) and dysregulated circadian gene expression (BMAL-1, CLOCK), both of which were mitigated by K6 supplementation. In the intestine, hypothalamus, and hippocampus, SD or SD combined with exercise-induced inflammation (TNF-α, IL-1β) and tight junction hyperpermeability (Claudin-1, ZO-1) were alleviated with K6 supplementation, as were the circadian genes (BMAL-1, CLOCK) and corticotropin-releasing hormone receptor genes (CRF1, CRF2) in hypothalamus and hippocampus under SD alone or combined with exercise. The functional probiotic K6 improved physiological adaption, neuropsychological behaviors, and exercise performance with the implementation of SD and exercise training, potentially through regulation of inflammation, circadian rhythm, and stress response, contributing to overall health maintenance. The K6 probiotic strain may serve as a nutritional strategy to mitigate health risks and enhance performance affected by sleep deprivation.