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The effect of COVID-19 lockdown on mental health, gut microbiota composition and serum cortisol levels.
The aim of this study was to assess changes in mental health, gut microbiota composition, and stress marker serum cortisol due to COVID-19 lockdown in asymptomatic individuals. Healthy adults participated in anthropometric measurements, blood and stool sample collection pre-lockdown and post-lockdown (n = 38, 63.2% females), lifestyle and psychological questionnaires were included in pre-lockdown measurement and lockdown survey (n = 46, 67.4% females). Subjects reported significantly higher body dissatisfaction (p = 0.007) and anxiety (p = 0.002), and significantly lower positive affect (p = 0.001) during lockdown compared with pre-lockdown. According to perceived stress, 51.6% of females and 20% of males experienced moderate to high stress. This was reflected in serum cortisol levels that significantly increased only in females (p = 0.006) post-lockdown and correlated with perceived stress (p = 0.037) and anxiety (p = 0.031). In addition to psychological measures, changes in gut microbiota composition were observed. Gut microbial alpha diversity significantly decreased (p = 0.033), whereas relative abundance of Proteobacteria significantly increased (p = 0.043) post-lockdown. Depression during lockdown was moderately positively correlated with changes in Bacteroidetes abundance (p = 0.015) and negatively with changes in Firmicutes abundance (p = 0.008). Alistipes abundance post-lockdown was moderately positively correlated with anxiety (p = 0.004) and negative affect (p = 0.005) during lockdown. Despite a small sample size and not being able to perform objective measurements during lockdown, the results confirm the effect of lockdown on mental health and gut microbiota composition that could have a great impact on our health (ClinicalTrials identifier: NCT04347213).
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Indolic Structure Metabolites as Potential Biomarkers of Non-infectious Diseases.
Interest in indolic structure metabolites, including a number of products of microbial biotransformation of the aromatic amino acid tryptophan, is increasingly growing. The review prepared by a team of authors is based on in-depthscrutiny of data available in PubMed, Scopus, Cyberleninka, Clinical Trials, and Cochrane Library, eventually narrowing the search to a set of keywords such as tryptophan metabolites; plasma metabolomics profiling; metabolomics fingerprinting; gas-, liquid chromatography mass spectrometry; serotonin; melatonin; tryptamine; indoxyl sulfate; indole-3-acetic acid; indole-3-propionic acid; 5-hydroxyindole-3-acetic acid; gut microbiota and microbial metabolites. It provides a summary that outlines the pattern of changes in the level of indolic structure metabolites in a number of diseases and deals with the data from the field of human microbiota metabolites. In modern experimental studies, including the use of gnotobiological (germ-free) animals, it has been convincingly proved that the formation of tryptophan metabolites such as indole-3-acetic acid, indole-3-propionic acid, tryptamine, and indoxyl sulfate is associated with gut bacteria. Attention to some concentration changes of indolic compounds is due to the fact that pronounced deviations and a significant decrease of these metabolites in the blood were found in a number of serious cardiovascular, brain or gastrointestinal diseases. The literature-based analysis allowed the authors to conclude that a constant (normal) level of the main metabolites of the indolic structure in the human body is maintained by a few strict anaerobic bacteria from the gut of a healthy body belonging to the species of Clostridium, Bacteroides, Peptostreptococcus, Eubacteria, etc. The authors focus on several metabolites of the indolic structure that can be called clinically significant in certain diseases, such as schizophrenia, depression, atherosclerosis, colorectal cancer, etc. Determining the level of indole metabolites in the blood can be used to diagnose and monitor the effectiveness of a comprehensive treatment approach.
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Autism-Associated Gut Microbiota-Derived Enterococcus facium Modulates Gut-Brain Axis Function and Behavior in Mice.
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social communication deficits, repetitive behaviors, and restricted interests. Although its pathogenesis is not fully understood, emerging evidence suggests a connection between gut microbiota alterations and ASD. The role of specific bacterial species, particularly Enterococcus faecium, in the development of ASD remains unclear. This study aimed to investigate the impact of E. faecium derived from the feces of autistic children on mice. Thirty male BALB/c mice were divided into three groups: control, E. coli, and E. faecium treatment groups. E. faecium was administered orally for 30 days. Behavioral assessments, including open field tests, sucrose preference, Y-maze, and social interaction tests, were performed to evaluate anxiety, depression, memory, and social behavior. Additionally, serum 5-HT levels were measured, and colon and brain tissues were analyzed for inflammation, blood-brain barrier (BBB) integrity, and histological changes. Stool DNA sequencing was used to assess microbiota diversity and composition. Treatment with E. faecium significantly altered behavior in mice, including increased anxiety, depression, impaired memory, and social dysfunction. Colon histology revealed severe damage, including increased inflammation, reduced tight junction protein expression, and decreased mucin-2 levels. Elevated serum lipopolysaccharide (LPS) levels indicated systemic inflammation, and gut microbiota analysis showed significant dysbiosis. In the brain, particularly within the hippocampus and cortical regions, E. faecium induced neural damage, heightened inflammation, and compromised blood-brain barrier integrity. Enterococcus faecium from autistic patients can induce significant behavioral changes in mice, potentially via gut microbiota dysbiosis, intestinal barrier disruption, and brain inflammation. These findings suggest that E. faecium may contribute to gut-brain axis dysregulation in ASD, although further mechanistic studies are warranted.
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Distinct gut microbiota profiles and network properties in older Korean individuals with subjective cognitive decline, mild cognitive impairment, and Alzheimer's disease.
BACKGROUND: The gut microbiota may influence cognitive function via the gut-brain axis. This study aimed to investigate the gut microbiota profiles of 346 older Korean individuals with subjective cognitive decline but no symptoms (SCD), mild cognitive impairment (MCI), or Alzheimer’s disease (AD). METHODS: Participants aged an average of 72.3 years underwent the profiling of cognitive function, amyloid-β (Aβ) deposition, apolipoprotein E (APOE) genetic variants, depression status, nutrition, and lifestyles. Human fecal bacterial FASTA/Q data (SCD, n = 24; MCI, n = 246; AD, n = 76) were processed using Quantitative Insights Into Microbial Ecology 2 (QIIME2) tools. Operational taxonomic units (OTUs) and their counts were assigned with the National Center for Biotechnology Information Basic Local Alignment Search Tool (BLAST). Machine learning models (random forest and XGBoost) identified key bacterial taxa differentiating groups. RESULTS: Redundancy analysis revealed associations between gut microbiota composition and cognitive function, age, gender, nutritional status, and body mass index. All three groups shared 71 common bacterial genera with distinct taxonomic profiles across cognitive states. The AD group uniquely harbored Hominisplanchenecus and Lentihominibacter, while the SCD group exclusively contained Anaerosacchariphilus and Anaerobutyricum. Phascolarctobacterium was shared between the AD and MCI groups, and Anaerostipes between the MCI and SCD groups. The SCD group showed significantly elevated Bifidobacterium catenulatum, Anaerobutyricum hallii, and Anaerostipes hadrus. Network analysis demonstrated greater microbial community complexity in the SCD group compared to the MCI and AD groups. Gut bacteria correlated with depression, Aβ deposition, APOE status, and cognitive scores. CONCLUSIONS: This study identified distinct gut microbiota profiles associated with different stages of cognitive impairment in older Korean adults. The observed associations between gut bacterial composition and cognitive function, neurodegeneration biomarkers, and related clinical factors suggest potential relationships that warrant further investigation. These findings contribute to the growing understanding of gut-brain interactions in cognitive aging.
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Gut microbiota decreased inflammation induced by chronic unpredictable mild stress through affecting NLRP3 inflammasome.
Dysbiosis of the gut microbiota is associated with the development of depression, but the underlying mechanism remains unclear. The aim of this study was to determine the relationship between microbiota and NLRP3 inflammasome induced by chronic unpredictable mild stress (CUMS). Fecal transplantation (FMT) experiment was conducted to elucidate the potential mechanism. Levels of NLRP3 inflammasome, microbiota, inflammatory factors and tight junction proteins were measured. CUMS stimulation significantly increased the levels of NLRP3, Caspase-1 and ASC in brain and colon(p<0.05), decreased the levels of tight junction proteins Occludin and ZO-1 (p<0.05). Interestingly, increased NLRP3 inflammasome and inflammatory cytokines and decreased tight junction proteins were found in antibiotic-treated (Abx) rats received CUMS rat fecal microbiota transplantation. Furthermore, fecal microbiota transplantation altered the microbiota in Abx rats, which partially overlapped with that of the donor rats. Importantly, probiotic administration amended the alteration of microbiota induced by CUMS treatment, then reduced the levels of NLRP3 inflammasome and inflammatory factors. In conclusion, these findings suggested that depression-like behaviors induced by CUMS stimulation were related to altered gut microbiota, broke the intestinal barrier, promoted the expression of NLRP3 inflammasome and elevated inflammation. Therefore, improving the composition of microbiota via probiotic can attenuate inflammation by amending the microbiota and suppressing the activation of NLRP3 inflammasome, which is considered as a novel therapeutic strategy for depression.
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Sex, Symptom Severity, and Quality of Life in Rheumatology.
Inflammatory rheumatic diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) show a striking female predominance ranging from 3:1 in RA up to 9:1 in SLE. The background for those gender bias is not fully understood yet, but seems to be the result of a complex interaction between sex hormones, (epi-)genetics, and possibly even the composition of gut microbiota. Moreover, time of disease onset, the clinical phenotype including co-morbidities as well as the course of the diseases during life differ between genders. The patient's sex therefore plays an emerging role for individual therapy decisions and co-morbidity screening in rheumatologic care. Male lupus patients, for example, tend to show more severe features such as renal involvement, pleurisy, and serositis, when being compared to female patients. Among RA patients, women are more likely to acquire conditions like thyroid dysfunctions, fibromyalgia, and depression than their male counterparts. These examples emphasize the importance of the patient's gender for the clinical routine and the resulting implications for prevention and therapy. The present article is going to review potential causes for the female predominance of rheumatic diseases and will examine the gender's impact on the disease phenotype, symptom severity, co-morbidities, and quality of life. For reasons of scope, the focus will be on RA and SLE as two of the most important rheumatic diseases with a large socioeconomic impact on society due to their incidence as well as mortality.
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[Surgical treatment of obesity from the nutritional point - opportunities and dangers].
Obesity is a civilization disease, which occurrence in the world population is gradually increasing. The basic causes of obesity include a sedentary lifestyle and energy-rich diet contributing to a positive energy balance. Methods of curing obesity contain the lifestyle modification, the pharmacological treatment and the surgical treatment. The bariatric surgery is a therapy that can be used among patients with BMI ≥40 or BMI ≥35 kg/m2 with comorbidities, e.g. hypertension, for whom previous treatment has been ineffective. The surgical treatment includes restrictive, limiting absorption and hybrid methods among them the most frequently performed sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB). Surgical treatment affects the clinical course of many chronic diseases, e.g. diabetes mellitus type 2. Unfortunately, this method of treatment is related to complications and is associated with increased risk of many complications, nutritional deficiencies, as well as deterioration of mental health. The potential causes of psychiatric disorders following bariatric surgery include dysbiosis and brain - gut axis dysfunction. After surgery, a dysbiosis is noticed (a reduction of Bifidobacterium spp.) that may increase the risk of depressive disorders occurrence. For this reason, to effective obesity treatment, patients undergoing bariatric surgery should be covered by the longterm care of an interdisciplinary team.
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Probiotic modulation of central and peripheral sensitization in a migraine model via the gut-brain-trigeminal axis.
The gut-brain axis has emerged as a pivotal modulator of migraine pathophysiology. This study examined the neurophysiological effects of targeted probiotic supplementation-Lactobacillus plantarum, Bifidobacterium longum, their combination, and a multi-strain formulation (Pro-14)-in a rat model of cortical spreading depression (CSD), a hallmark trigger of migraine. B.longum significantly reduced CSD frequency (p = 0.0045), while L.plantarum and its combination with B.longum markedly attenuated CSD amplitude (p = 0.0003, p = 0.01, respectively), reflecting suppression of cortical hyperexcitability. In small-to-medium-sized trigeminal ganglion (TG) neurons, probiotics significantly lowered total spike counts (p < 0.0001), and induced hyperpolarization of resting membrane potential (p < 0.0001), consistent with peripheral desensitization. Additionally, the threshold-Resting Membrane Potential (RMP) gap increased significantly across all treated groups (p < 0.0001), indicating reduced neuronal excitability. Only B.longum prolonged action potential duration and depolarization time (p = 0.0454 and p = 0.034, respectively), suggesting enhanced modulation of nociceptive signaling. In large-sized TG neurons, similar hyperpolarizing trends in RMP (p < 0.0001) and increased excitability thresholds (p < 0.0001) were observed without changes in spike frequency. These findings reveal strain-specific modulation of central and peripheral sensitization via the gut-brain-trigeminal axis and support the development of precision-targeted, microbiota-based therapies as non-pharmacologic strategies for migraine prophylaxis.
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Estradiol-mediated protection against high-fat diet induced anxiety and obesity is associated with changes in the gut microbiota in female mice.
Decreased estrogens during menopause are associated with increased risk of anxiety, depression, type 2 diabetes and obesity. Similarly, depleting estrogens in rodents by ovariectomy, combined with a high-fat diet (HFD), increases anxiety and adiposity. How estrogens and diet interact to affect anxiety and metabolism is poorly understood. Mounting evidence indicates that gut microbiota influence anxiety and metabolism. Here, we investigated the effects of estradiol (E) and HFD on anxiety, metabolism, and their correlation with changes in gut microbiota in female mice. Adult C57BL/6J mice were ovariectomized, implanted with E or vehicle-containing capsules and fed a standard diet or HFD. Anxiety-like behavior was assessed and neuronal activation was measured by c-fos immunoreactivity throughout the brain using iDISCO. HFD increased anxiety-like behavior, while E reduced this HFD-dependent anxiogenic effect. Interestingly, E decreased neuronal activation in brain regions involved in anxiety and metabolism. E treatment also altered gut microbes, a subset of which were associated with anxiety-like behavior. These findings provide insight into gut microbiota-based therapies for anxiety and metabolic disorders associated with declining estrogens in menopausal women.
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Dysbiosis and fecal microbiota transplant: Contemplating progress in health, neurodegeneration and longevity.
The gut-brain axis plays an important role in mental health. The intestinal epithelial surface is colonized by billions of commensal and transitory bacteria, known as the Gut Microbiota (GM). However, potential pathogens continuously stimulate intestinal immunity when they find the place. The last two decades have witnessed several studies revealing intestinal bacteria as a key factor in the health-disease balance of the gut, as well as disease-emergent in other parts of the body. Various neurological processes, such as cognition, learning, and memory, could be affected by dysbiosis in GM. Additionally, the aging process and longevity are related to systemic inflammation caused by dysbiosis. Commensal GM affects brain development, behavior, and healthy aging suggesting that building changes in GM might be a potential therapeutic method. The innovation in GM dysbiosis is intervention by Fecal Microbiota Transplantation (FMT), which has been confirmed as a therapy for recurrent Clostridium difficile infections and is promising for other clinical disorders, such as Parkinson's disease, Multiple Sclerosis (MS), Alzheimer's disease, and depression. Additionally, FMT may be possible to promote healthy aging, and extend longevity. This review aims to connect dysbiosis, neurological disorders, and aging and the potential of FMT as a therapeutic strategy to treat these disorders, and to enhance the quality of life in the elderly.