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Alterations of oral microbiota in patients with panic disorder.
The main characteristics of panic disorder (PD) include recurrent panic attacks and persistent worry, accompanied by other physical and cognitive symptoms. While recent studies have revealed that gut bacteria play an important role in anxiety and depression, little is known about the relationship between oral microbiota and PD. Therefore, the objective of this study was to explore a possible correlation between oral microbiota and PD. We conducted 16S rRNA sequencing to compare differences in the oral microbiota of patients with PD (n = 26) and healthy controls (n = 40). Patients with PD exhibited higher alpha diversity (abundance and evenness) in their oral microbiota than healthy controls, while analysis of beta diversity revealed that the two groups differed in microbial community composition. Moreover, the relative abundance of 61 genera differed between them. Overall, PD resulted in distinct oral microbial profiles that could be potential diagnostic markers and therapeutic targets.
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Transport stress alters serum biochemistry and gut microbiota in Tibetan sheep (ovis aries): a 30-day recovery assessment.
BACKGROUND: Transport stress poses a major challenge to the livestock industry. Studies have shown that transportation stress can cause depression, elevated body temperature and dysbiosis of intestinal microbiota in meat goats, and in severe cases, even lead to death of the animals, which in turn affects the economic efficiency of the farming industry. However, the changes in blood biochemical indicators and flora of Tibetan sheep throughout the receiving period after long-distance transport remain unclear. METHODS: In this study, six 7-month-old Tibetan sheep with similar body weights were selected for a 30-d transport trial, and blood and faecal samples were collected for blood biochemical indices and 16 S microbiome sequencing before transport (BT), and on day 1 (AT 1), day 16 (AT 16), and day 30 (AT 30) after the end of the transport, respectively. RESULT: And a number of blood biochemical indices (creatine kinase (CK), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate aminotransferase (AST), cortisol (COR), and adrenocorticotropic hormone (ACTH)) were significantly elevated (P < 0.05). Combined analysis of physiological and biochemical indices with 16 S rDNA sequencing showed that Turicibacter, Romboutsia and Clostridium_sensu_stricto_1 were positively correlated with LDH, ALP, CK, AST, and ACTH, while Prevotellaceae_UCG_004 was negatively correlated. Furthermore, the observed recovery trends in vital signs after AT 16 suggest that Tibetan sheep may be able to adapt to the new environment within one month post-transport. The present study illustrated the effects of transport without measures on the vital signs, serum biochemical indicators and faecal microorganisms of Tibetan sheep throughout the receiving period, which is of great significance in guiding the transport of Tibetan sheep and solving the damage caused by transport stress on the economic benefits of the farming industry.
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TGR5 is essential for protecting from chronic stress-induced learning and memory impairments in mice by modulating inflammation associated with the gut-brain axis.
BACKGROUND: CS impairs brain function, causing long-term changes in neural systems linked to anxiety, depression, and cognition. TGR5 is a key receptor crucial for modulating various physiological processes, impacting metabolic homeostasis and inflammation. However, the role of TGR5 in regulating CS-induced learning and memory impairments along the gut-brain axis remains incompletely understood. METHODS: WT and TGR5 KO male C57BL/6J mice underwent 21-day chronic restraint stress to model stress-induced memory deficit. Stress severity and cognitive function were evaluated by behavioral tests. Hippocampal and intestinal integrity were assessed by H&E, Nissl, AB-PAS staining, and TEM ultrastructural analysis. CORT and 5-HT levels were quantified by ELISA. BAs and gut microbiota were profiled by UPLC-MS/MS and 16S rRNA sequencing. Hippocampal and colonic transcriptomes were analyzed by RNA-seq. Electrophysiological LTP was recorded in hippocampal CA1. Inflammatory cytokines were detected by qPCR. Fkbp51, TGR5, and LCN2 proteins were quantified by Western blot, while TGR5 and LCN2 were localized by IHC/IF. RESULTS: This study found that 21 days of CRS suppressed body weight gain, triggered anxiety-like behaviors, and impaired spatial learning and memory in mice. CS induced significant damage to the hippocampal CA1 region and colon, accompanied by elevated TGR5 expression in both tissues. Moreover, CS altered gut microbiota composition and BAs metabolism (most notably increasing TCDCA levels) potentially contributing to neuroinflammation along the gut-brain axis. Using TGR5 KO mice, this study demonstrated that TGR5 deficiency exacerbated CS-induced hippocampal neuroinflammation, as evidenced by increased expression of pro-inflammatory markers including IL-1β, IL-6, TNF-α, and LCN2. CS also induced decreased 5‑HT levels and severely impaired LTP, disrupting synaptic plasticity and neurotransmission, which ultimately led to learning and memory deficits. In the colon, TGR5 deficiency similarly worsened CS-induced tissue injury. These findings highlight a protective role of TGR5 in both the hippocampus and the colon. CONCLUSIONS: In summary, TGR5 is essential for protecting from CS-induced learning and memory impairments in mice by modulating inflammation associated with the gut-brain axis.
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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.