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Longitudinal analysis of short-chain fatty acid profiles in stool of sleeve gastrectomy patients.
Obesity presents significant health risks, including metabolic disorders and depressive symptoms, necessitating effective interventions such as sleeve gastrectomy (SG), which enables substantial weight loss and metabolic improvements. The primary question of this study was whether SG also affects faecal short-chain fatty acid (SCFA) profiles over 12 months, and whether these changes are related to anthropometric, biochemical, and psychological parameters. A total of 37 female patients with obesity were included in this prospective, observational study. Patients underwent SG and were followed for 12 months postoperatively. SCFA profiles were analysed by gas chromatography-mass spectrometry (GC-MS). Faecal samples for SCFA analysis, anthropometric measurements, blood biochemical markers, food intake and psychological assessments were collected at baseline and at regular intervals after surgery. Our results indicate that SG leads to significant reductions in body mass index, lipid profiles, and systemic inflammation markers, with concurrent alterations in SCFA concentrations, particularly a decrease in major SCFAs (acetic, propionic, and butyric acids) over time. An increase in branched SCFAs was observed post-surgery, which may reflect shifts in the gut microbiota composition and fermentation processes. Patients also reported improvements in emotional well-being and dietary habits. These findings support the hypothesis that SG induces changes in gut microbiota metabolism and underscore the complex interplay between bariatric surgery, gut microbiota, SCFA metabolism, and psychological health. They highlight the need for further research to clarify the long-term implications of these changes and the mechanisms involved.
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Host associated probiotics Lactobacillus reuteri and Enterococcus faecium Mitigate multidrug resistant Salmonella enterica in broiler chicks.
Probiotics can provide an eco-friendly alternative solution to improve poultry production and disease resistance. Considering safer and more effective probiotic strains from cultured species, this study included three host-associated probiotics (HAPs): Limosilactobacillus reuteri PFS4, Enterococcus faecium PFS13, and PFS14, previously isolated from poultry gut. This study evaluated the effects of three HAPs blend and a commercial probiotic blend (ProtexinR) on broiler growth, intestinal morphology, serum immunoglobulins, and cecal microflora challenged with two fluoroquinolone-resistant Salmonella Typhimurium (ST) and Salmonella Enteritidis (SE). A total of 240-day-old broiler chicks were randomly assigned to six treatment groups (n = 40 in each group): negative control (NC), positive control (PC), HAPs control blend (IPRO-) without ST and SE challenge, HAPs blend with ST and SE challenge (IPRO+), Commercial probiotic (ProtexinR) blend with ST and SE challenge (CM+), Commercial probiotic (ProtexinR) control (CM-) blend without ST and SE challenge. Growth parameters, including body weight gain (BWG), average feed intake (AFI), and feed conversion ratio (FCR), along with microbial populations, were assessed weekly. Meanwhile, gut morphology, relative organ weight, and serum immunoglobulin levels were evaluated on days 7 and 28. The chicks infected with ST and SE were depressed, had high mortality (20 %), and reduced BWG. The growth performance parameters were significantly improved (p ≤ 0.005) in all groups administered probiotics, with the IPRO- group exhibiting the highest results. Similarly, light microscopy findings showed that all probiotic-fed groups significantly (p ≤ 0.005) improved their gut morphology compared to the positive control group. Both HAPs and commercial probiotic blend treatments increased serum IgA and IgG compared with the PC (p ≤ 0.001). IPRO+ treatment significantly (p ≤ 0.001) increased cecal populations of total Lactobacillus and total Enterococcus, while reducing cecal and liver populations of Salmonella. In conclusion, the use of HAPs showed better growth performance and enhanced MDR Salmonella control, suggesting that the poultry sector should prioritize the development and application of probiotics derived from host-specific strains rather than other sources.
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Ozone rectal insufflation mitigates chronic rapid eye movement sleep deprivation-induced cognitive impairment through inflammation alleviation and gut microbiota regulation in mice.
A range of sleep disorders has the potential to adversely affect cognitive function. This study was undertaken with the objective of investigating the effects of ozone rectal insufflation (O3-RI) on cognitive dysfunction induced by chronic REM sleep deprivation, as well as elucidating possible underlying mechanisms. O3-RI ameliorated cognitive dysfunction in chronic REM sleep deprived mice, improved the neuronal damage in the hippocampus region and decreased neuronal loss. Administration of O3-RI may protect against chronic REM sleep deprivation induced cognitive dysfunction by reversing the abnormal expression of Occludin and leucine-rich repeat and pyrin domain-containing protein 3 inflammasome as well as interleukin-1β in the hippocampus and colon tissues. Moreover, the microbiota diversity and composition of sleep deprivation mice were significantly affected by O3-RI intervention, as evidenced by the reversal of the Firmicutes/Bacteroidetes abundance ratio and the relative abundance of the Bacteroides genus. In particular, the relative abundance of the Bacteroides genus demonstrated a pronounced correlation with cognitive impairment and inflammation. Our findings suggested that O3-RI can improve cognitive dysfunction in sleep deprivation mice, and its mechanisms may be related to regulating gut microbiota and alleviating inflammation and damage in the hippocampus and colon.
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Intestinal microbiota imbalance resulted by anti-Toxoplasma gondii immune responses aggravate gut and brain injury.
BACKGROUND: Toxoplasma gondii infection affects a significant portion of the global population, leading to severe toxoplasmosis and, in immunocompromised patients, even death. During T. gondii infection, disruption of gut microbiota further exacerbates the damage to intestinal and brain barriers. Therefore, identifying imbalanced probiotics during infection and restoring their equilibrium can regulate the balance of gut microbiota metabolites, thereby alleviating tissue damage. METHODS: Vimentin gene knockout (vim-/-) mice were employed as an immunocompromised model to evaluate the influence of host immune responses on gut microbiota balance during T. gondii infection. Behavioral experiments were performed to assess changes in cognitive levels and depressive tendencies between chronically infected vim-/- and wild-type (WT) mice. Fecal samples were subjected to 16S ribosomal RNA (rRNA) sequencing, and serum metabolites were analyzed to identify potential gut probiotics and their metabolites for the treatment of T. gondii infection. RESULTS: Compared to the immunocompetent WT sv129 mice, the immunocompromised mice exhibited lower levels of neuronal apoptosis and fewer neurobehavioral abnormalities during chronic infection. 16S rRNA sequencing revealed a significant decrease in the abundance of probiotics, including several species of Lactobacillus, in WT mice. Restoring this balance through the administration of Lactobacillus murinus and Lactobacillus gasseri significantly suppressed the T. gondii burden in the intestine, liver, and brain. Moreover, transplantation of these two Lactobacillus spp. significantly improved intestinal barrier damage and alleviated inflammation and neuronal apoptosis in the central nervous system. Metabolite detection studies revealed that the levels of various Lactobacillus-related metabolites, including indole-3-lactic acid (ILA) in serum, decreased significantly after T. gondii infection. We confirmed that L. gasseri secreted much more ILA than L. murinus. Notably, ILA can activate the aromatic hydrocarbon receptor signaling pathway in intestinal epithelial cells, promoting the activation of CD8+ T cells and the secretion of interferon-gamma. CONCLUSION: Our study revealed that host immune responses against T. gondii infection severely disrupted the balance of gut microbiota, resulting in intestinal and brain damage. Lactobacillus spp. play a crucial role in immune regulation, and the metabolite ILA is a promising therapeutic compound for efficient and safe treatment of T. gondii infection.
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Characteristic alterations of gut microbiota and serum metabolites in patients with chronic tinnitus: a multi-omics analysis.
Chronic tinnitus is a central nervous system disorder. Currently, the effects of gut microbiota on tinnitus remain unexplored. To explore the connection between gut microbiota and tinnitus, we conducted 16S rRNA sequencing of fecal microbiota and serum metabolomic analysis in a cohort of 70 patients with tinnitus and 30 healthy volunteers. We used the weighted gene co-expression network method to analyze the relationship between the gut microbiota and the serum metabolites. The random forest technique was utilized to select metabolites and gut taxa to construct predictive models. A pronounced gut dysbiosis in the tinnitus group, characterized by reduced bacterial diversity, an increased Firmicutes/Bacteroidetes ratio, and some opportunistic bacteria including Aeromonas and Acinetobacter were enriched. In contrast, some beneficial gut probiotics decreased, including Lactobacillales and Lactobacillaceae. In serum metabolomic analysis, serum metabolic disturbances in tinnitus patients and these differential metabolites were enriched in pathways of neuroinflammation, neurotransmitter activity, and synaptic function. The predictive models exhibited great diagnostic performance, achieving 0.94 (95% CI: 0.85-0.98) and 0.96 (95% CI: 0.86-0.99) in the test set. Our study suggests that changes in gut microbiota could potentially influence the occurrence and chronicity of tinnitus, and exert regulatory effects through changes in serum metabolites. Overall, this research provides new perceptions into the potential role of gut microbiota and serum metabolite in the pathogenesis of tinnitus, and proposes the "gut-brain-ear" concept as a pathomechanism underlying tinnitus, with significant clinical diagnostic implications and therapeutic potential.IMPORTANCETinnitus affects millions of people worldwide. Severe cases may lead to sleep disorders, anxiety, and depression, subsequently impacting patients' lives and increasing societal healthcare expenditures. However, tinnitus mechanisms are poorly understood, and effective therapeutic interventions are currently lacking. We discovered the gut microbiota and serum metabolomics changes in patients with tinnitus, and provided the potential pathological mechanisms of dysregulated gut flora in chronic tinnitus. We proposed the innovative concept of the "gut-brain-ear axis," which underscores the exploration of gut microbiota impact on susceptibility to chronic tinnitus through serum metabolic profile modulation. We also reveal novel biomarkers associated with chronic tinnitus, offering a new conceptual framework for further investigations into the susceptibility of patients, potential treatment targets for tinnitus, and assessing patient prognosis. Subsequently, gut microbiota and serum metabolites can be used as molecular markers to assess the susceptibility and prognosis of tinnitus.Furthermore, fecal transplantation may be used to treat tinnitus.
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Stereotactic infusion of rotenone into the SN induced a late-stage model of Parkinson's disease.
The establishment of an in vivo model for Parkinson's disease (PD) that accurately mimics late-stage clinical features is crucial for elucidating disease pathogenesis and developing novel therapeutic strategies. To establish this model, rotenone (ROT) was stereotactically infused into the substantia nigra (SN). Motor behavior in PD mice was assessed using the pole test and rotarod test. Apomorphine (APO)-induced rotation and dystonia were also evaluated. Alterations in anxiety, depression, and cognitive function were examined using the open field test, sucrose preference test, Y-maze test, and Morris water maze test, respectively. Gastrointestinal (GI) motility was determined by examining the timing of pink stool passage. Changes in gut microbiota composition were analyzed via 16S rRNA sequencing. The expression and localization of nucleotide-binding oligomerization domain-leucine-rich repeat-pyrin domain-containing 3 (NLRP3), caspase-1, and α-synuclein (α-syn) within astrocytes were determined using immunofluorescence. Peripheral organ toxicity induced by ROT was investigated using hematoxylin and eosin (HE) staining. Experimental results demonstrated that the number of APO-induced rotations in the ROT group exceeded 210 rpm at 4 weeks and decreased significantly by 36 weeks, reflecting progressive disease characteristics. Specifically, the incidence of APO-induced dystonia was significantly higher in the ROT group at 36 weeks compared to 4 weeks (P < 0.05). Compared to the vehicle group, ROT-treated mice exhibited prolonged pole test descent time and reduced rotarod latency. The open field test revealed decreased center duration and crossings. Morris water maze showed fewer platform crossings and reduced target quadrant time. However, no statistically significant differences were observed between groups in the sucrose preference test at either 4 or 36 weeks. By 36 weeks, ROT-treated mice demonstrated a significantly lower spontaneous alternation rate compared to vehicle controls. ROT infusion also reduced overall gut microbiota abundance and altered microbial composition. Specifically, the ROT group showed decreased abundance of Allobaculum, Atopobium, Sneathia, Rikenella, Aestuariispira, Bacillus, Barnesiella, Escherichia/Shigella, Klebsiella, Eisenbergiella, and Parasutterella. Immunostaining analysis revealed that compared with the vehicle group, NLRP3, cleaved caspase-1, and α-syn expression was increased in astrocytes in the ROT group. The ROT-based model reproduced the clinical features of the early and late stages of PD, particularly dystonia and inflammasome activation, thus providing a reliable framework for studying late-stage PD.
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Systematic Review of Gut Microbiota and Major Depression.
Background: Recently discovered relationships between the gastrointestinal microbiome and the brain have implications for psychiatric disorders, including major depressive disorder (MDD). Bacterial transplantation from MDD patients to rodents produces depression-like behaviors. In humans, case-control studies have examined the gut microbiome in healthy and affected individuals. We systematically reviewed existing studies comparing gut microbial composition in MDD and healthy volunteers. Methods: A PubMed literature search combined the terms "depression," "depressive disorder," "stool," "fecal," "gut," and "microbiome" to identify human case-control studies that investigated relationships between MDD and microbiota quantified from stool. We evaluated the resulting studies, focusing on bacterial taxa that were different between MDD and healthy controls. Results: Six eligible studies were found in which 50 taxa exhibited differences (p < 0.05) between patients with MDD and controls. Patient characteristics and methodologies varied widely between studies. Five phyla-Bacteroidetes, Firmicutes, Actinobacteria, Fusobacteria, and Protobacteria-were represented; however, divergent results occurred across studies for all phyla. The largest number of differentiating taxa were within phylum Firmicutes, in which nine families and 12 genera differentiated the diagnostic groups. The majority of these families and genera were found to be statistically different between the two groups in two identified studies. Family Lachnospiraceae differentiated the diagnostic groups in four studies (with an even split in directionality). Across all five phyla, nine genera were higher in MDD (Anaerostipes, Blautia, Clostridium, Klebsiella, Lachnospiraceae incertae sedis, Parabacteroides, Parasutterella, Phascolarctobacterium, and Streptococcus), six were lower (Bifidobacterium, Dialister, Escherichia/Shigella, Faecalibacterium, and Ruminococcus), and six were divergent (Alistipes, Bacteroides, Megamonas, Oscillibacter, Prevotella, and Roseburia). We highlight mechanisms and products of bacterial metabolism as they may relate to the etiology of depression. Conclusions: No consensus has emerged from existing human studies of depression and gut microbiome concerning which bacterial taxa are most relevant to depression. This may in part be due to differences in study design. Given that bacterial functions are conserved across taxonomic groups, we propose that studying microbial functioning may be more productive than a purely taxonomic approach to understanding the gut microbiome in depression.
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Plasma cytokine levels in patients with chronic alcohol overconsumption: Relations to gut microbiota markers and clinical correlates.
BACKGROUND: Alcohol-related morbidity may involve changes in the gut microbiota and immune dysregulation. We have previously demonstrated alterations in gut microbiota composition and functions in patients with alcohol overconsumption, and now aimed to investigate possible associations between cytokine levels, gut microbiota, and clinical symptoms. METHODS: We included hospital inpatients with a history of chronic alcohol overconsumption. For comparison, we included control patients with a low alcohol intake. Cytokine levels (TGF-β1, TNF-α, IL-10, IL-8, IL-6, IFN-γ, MCP-1, IL-1RA, IL-1β, and IL-17) were determined using a customized V-plex assay. We then examined associations of cytokine levels with the abundance of Proteobacteria and Faecalibacterium, percentage of the short-chain fatty acid butyrate, psychiatric symptoms (Hospital Anxiety and Depression Scale), and biochemical liver variables. RESULTS: We included 28 patients with alcohol overconsumption (79% men), and 25 control patients (72% men). Patients with alcohol overconsumption had higher levels of IL-6 (p = 0.002), IFN-γ (p = 0.018), and MCP-1 (p = 0.006), and lower levels of TGF-β1 (p = 0.017) compared with control patients. Inverse correlations were found between Proteobacteria abundance and TNF-α (Rs = -0.55, p = 0.02) and IL-8 (Rs = -0.58, p = 0.014), and between Faecalibacterium and MCP-1 levels (Rs = -0.56, p = 0.02) in the control patients, but not in patients with alcohol overconsumption. Patients with alcohol overconsumption reported more psychiatric symptoms, and these symptoms were inversely correlated with IL-10 levels. There were positive correlations between several of the assessed cytokines and biochemical liver variables, and negative correlations between cytokine levels and albumin. CONCLUSION: Patients with alcohol overconsumption had a cytokine profile suggestive of increased systemic inflammatory activity, with higher levels of pro-inflammatory cytokines (IL-6, IFN-γ, and MCP-1) and lower levels of anti-inflammatory cytokines (TGF-β1). The findings may represent a link between alcohol use and alcohol-related morbidity.
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Far-Infrared Therapy Based on Graphene Ameliorates High-Fat Diet-Induced Anxiety-Like Behavior in Obese Mice via Alleviating Intestinal Barrier Damage and Neuroinflammation.
The consumption of a high-fat diet (HFD) has been implicated in the etiology of obesity and various neuropsychiatric disturbances, including anxiety and depression. Compelling evidence suggests that far-infrared ray (FIR) possesses beneficial effects on emotional disorders. However, the efficacy of FIR therapy in addressing HFD-induced anxiety and the underlying mechanisms remain to be elucidated. Here, we postulate that FIR emitted from a graphene-based therapeutic device may mitigate HFD-induced anxiety behaviors. The graphene-FIR modify the gut microbiota in HFD-mice, particularly by an enriched abundance of beneficial bacteria Clostridiaceae and Erysipelotrichaceae, coupled with a diminution of harmful bacteria Lachnospiraceae, Anaerovoracaceae, Holdemania and Marvinbryantia. Graphene-FIR also improved intestinal barrier function, as evidenced by the augmented expression of the tight junction protein occludin and G protein-coupled receptor 43 (GPR43). In serum level, we observed the decreased free fatty acids (FFA), lipopolysaccharides (LPS), diamine oxidase (DAO) and D-lactate, and increased the glucagon-like peptide-2 (GLP-2) levels in graphene-FIR mice. Simultaneously, inflammatory cytokines IL-6, IL-1β, and TNF-α manifested a decrease subsequent to graphene-FIR treatment in both peripheral and central system. Notably, graphene-FIR inhibited over expression of astrocytes and microglia. We further noticed that the elevated the BDNF and decreased TLR4 and NF-κB expression in graphene-FIR group. Overall, our study reveals that graphene-FIR rescued HFD-induced anxiety via improving the intestine permeability and the integrity of blood-brain barrier, and reduced inflammatory response by down regulating TLR4/NF-κB inflammatory pathway.
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Fluoxetine attenuates the anxiolytic effects of the probiotic VSL#3 in a stress-vulnerable genetic line of aves in the chick social-separation stress test, a dual screening assay.
Anxiety disorders represent one of the most common and debilitating illnesses worldwide. However, the development of novel therapeutics for anxiety disorders has lagged compared to other mental illnesses. A growing body of research suggests the gut microbiota plays a role in the etiopathology of anxiety disorders and may, therefore, serve as a novel target for their treatment through the use of probiotics. The use of dietary supplements like probiotics is increasing and their interaction with pharmacotherapies is not well understood. Utilizing the chick social-separation stress test, the primary aim of this study was to evaluate the commercially-available multi-strain probiotic found in VSL#3 for potential anxiolytic-like and/or antidepressant-like effects in the stress-vulnerable Black Australorp genetic line. A secondary aim was to evaluate the interaction between probiotics and the SSRI fluoxetine. Animals were treated with either saline, probiotics, fluoxetine, or probiotics + fluoxetine for 8 days prior to exposure to a 90-min isolation stressor that produces both a panic-like (i.e., anxiety-like) state followed by a state of behavioral despair (i.e., depression-like). The 8-day probiotic regimen produced anxiolytic-like effects but did not attenuate behavioral despair. Fluoxetine failed to significantly alter behavior in either of the two phases. Moreover, the combination of fluoxetine with probiotics attenuated the anxiolytic-like effects of probiotics. The fluoxetine + probiotics combination had no effect on behavioral despair. The results of the current study align with other preclinical studies and some clinical trials suggesting probiotics may offer beneficial effects on anxiety. Investigations examining the anxiolytic-like mechanism of probiotics are needed before any conclusions can be made. Additionally, as the use of probiotics becomes more popular, research on the interactions between probiotic-microbiota and psychotropic medications is necessary.