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The Brain-Gut Axis and Stress in Inflammatory Bowel Disease.
The brain-gut axis serves as a circuit that incorporates the human experience, the state of mind, the gut microbiome, and the immune response that ultimately drives the phenotypic expression of inflammatory bowel disease (IBD). There are several biological pathways through which stress can play a deleterious role, including through increasing intestinal permeability, which can facilitate intestinal translocation of bacteria. Stress has an impact on symptoms in IBD; however, there is limited evidence that stress triggers increased intestinal inflammation. Although attention to stress and psychiatric comorbidity is important in the management of IBD, there are few clinical trials to direct management.
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Meta-Analysis of the Gut Microbiome: An African American Representation.
The human gut hosts approximately 100 trillion microbes, forming a complex ecosystem critical to the body's metabolism, nutrition, and immune function. Despite growing research, African Americans remain underrepresented in clinical studies. This study addresses the gap through a comprehensive meta-analysis of gut microbiome datasets. Fecal sample data from amplicon sequencing were analyzed using a bioinformatics pipeline that incorporated DADA2 for sequence processing and Phyloseq for diversity analysis within RStudio (v2024.09.0+375). Statistical approaches, including Wilcoxon tests, Kruskal-Wallis tests, PERMANOVA, and ANCOM-BC, identified significant microbial differences. Results revealed that African Americans exhibited lower microbial diversity. Beta diversity metrics demonstrated a stronger effect of ethnicity compared to diet, age, sex, and BMI, highlighting its significance in microbiome variation. Similarly, ANCOM-BC identified Clostridium sensu stricto 1 significantly enriched in healthy African Americans, while Dialister was depleted, a finding with potential clinical relevance given previous research linking reduced Dialister abundance with depression. Additionally, machine learning approaches were found to potentially complement traditional statistical methods by handling class imbalance and identifying complex microbial associations. By addressing critical gaps in microbiome research, this study underscores the importance of inclusive datasets in enhancing disease risk prediction and ensuring that microbiome-based health interventions are equitable and broadly applicable.
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Unraveling the role of the gut microbiome in pregnancy disorders: insights and implications.
The gut microbiota is the collective term for the microorganisms that reside in the human gut. In recent years, advances in sequencing technology and bioinformatics gradually revealed the role of gut microbiota in human health. Dramatic changes in the gut microbiota occur during pregnancy due to hormonal and dietary changes, and these changes have been associated with certain gestational diseases such as preeclampsia (PE) and gestational diabetes mellitus (GDM). Modulation of gut microbiota has also been proposed as a potential treatment for these gestational diseases. The present article aims to review current reports on the association between gut microbiota and gestational diseases, explore possible mechanisms, and discuss the potential of probiotics in gestational diseases. Uncovering the link between gut microbiota and gestational diseases could lead to a new therapeutic approach.
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Associations between disordered gut microbiota and changes of neurotransmitters and short-chain fatty acids in depressed mice.
Mounting evidence suggests that gut microbiota can play an important role in pathophysiology of depression, but its specific molecular mechanisms are still unclear. This study was conducted to explore the associations between changes in neurotransmitters and short-chain fatty acids (SCFAs) and altered gut microbiota in depressed mice. Here, the chronic restraint stress (CRS) model of depression was built. The classical behavioral tests were conducted to assess the depressive-like behaviors of mice. The 16S rRNA gene sequence extracted from fecal samples was used to assess the gut microbial composition. Liquid and gas chromatography mass spectroscopy were used to identify neurotransmitters in hypothalamus and SCFAs in fecal samples, respectively. Finally, 29 differential bacteria taxa between depressed mice and control mice were identified, and the most differentially abundant bacteria taxa were genus Allobaculum and family Ruminococcaceae between the two groups. The acetic acid, propionic acid, pentanoic acid, norepinephrine, 5-HIAA and 5-HT were significantly decreased in depressed mice compared to control mice. Genus Allobaculum was found to be significantly positively correlated with acetic acid and 5-HT. Taken together, these results provided novel microbial and metabolic frameworks for understanding the role of microbiota-gut-brain axis in depression, and suggested new insights to pave the way for novel therapeutic methods.
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PECULIARITIES OF THE GUT MICROBIOTA IN PATIENTS WITH MIGRAINE COMPARING TO HEALTHY INDIVIDUALS.
OBJECTIVE: The aim: Analyze the gut microbiome state in patients with migraine (M) and healthy individuals, to assess possible correlations between the detected changes in patients with migraine and the frequency, intensity of headaches, psycho-emotional state of the patients, and their quality of life. PATIENTS AND METHODS: Materials and methods: 100 objects were enrolled, divided into 2 groups: main - patients with M and control - healthy volunteers. Investigation of the intestinal microbiome was performed by chromato-mass spectrometry. For M patients the following scales were used: Visual Analogue Scale (VAS), Migraine Disability Assessment (MIDAS), Back Depression Inventory (BDI). RESULTS: Results: In main group increased amount of Alcaligenes spp (p = 0.0061), Clostridium coccoides (p = 0.0021), Clostridium propionicum (p = 0.0287), Eggerthella lenta (p = 0.0138), Pseudonocardia spp (p = 0.0210), Rhodococcus spp (p = 0.0164), Candida spp (p = 0.0079), Micromycetes spp (campesterol) (p = 0.0011) were found. Patients with M had a raised amount of Herpes simplex (p = 0.0305) and endotoxin level (p = 0.0459). Differences in gut microorganisms in both groups were significant. In patients with M negative correlations were observed between Alcaligenes spp ammount and BDI score (r = -0.6226, p =0.007), VAS score (r = -0.489, p = 0.046), headache frequency (r = -0.487, p = 0.046); between the levels of Clostridium coccoides and MIDAS score (r =-0.51, p = 0.035), BDI score (r = -0.54, p = 0.025) and positive correlation between Eggerthella lenta level and VAS score (r =0.4830, p=0.049). CONCLUSION: Conclusions: Correlations between changes of gut microbiome and M are promising for further research.
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Implications of the gut microbiota in vulnerability to the social avoidance effects of chronic social defeat in male mice.
Appreciable evidence suggests that perturbations within the gut microbiome and the immune system may play a key role in the pathogenesis of depression stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with social avoidance behaviors, a feature of depression, and pro-inflammatory variations among socially stressed mice. Male C57BL/6 mice experienced social defeat or a control condition once a day for 10 consecutive days. Social avoidance behaviors were examined three weeks after the last defeat or control episode and blood, brain, and cecum contents were collected 24h afterward for the determination of corticosterone, pro-inflammatory cytokines, and microbial populations. Mice that were most susceptible to the behavioral effects of chronic social defeat (reflected by severe social avoidance behaviors) displayed the greatest changes within particular sets of bacteria at the phylum and genus taxonomic ranks. Although plasma and brain cytokines were not significantly altered in socially defeated mice, changes in the mRNA expression of interleukin (IL)-1β and IL-6 within the prefrontal cortex were associated with elevated abundance of Flavobacterium spp. and reduced abundance of Turicibacter spp., which were also strongly correlated to social avoidance severity. Although at this time a causal connection cannot be inferred, these results point to the possibility that specific clusters of bacterial communities in cecum contents may be linked to vulnerability to social deficits stemming from prolonged social stressor experiences.
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Early life adversity promotes a milieu in favor of catabolic bone turnover in females: Mycobacterium vaccae NCTC 11659 proofs protective in preclinical studies.
Despite early clinical studies supporting the hypothesis that early life adversity (ELA) negatively affects the bone and despite typical ELA-associated disorders, including post-traumatic stress disorder (PTSD) and major depressive disorder (MD), are associated with osteoporosis and increased bone fracture risk, preclinical studies do not support this association. However, previous studies were only conducted in male but not female mice. In the current study we showed that ELA, induced by the classical maternal separation (MS) paradigm, facilitated femoral osteoclast activity specifically in female but not male mice. This was associated with a transient decline in both intestinal alpha diversity and Firmicutes/Bacteroidetes ratio, suggesting that the microbiome-gut-bone axis is involved in these effects. Moreover, ELA long-lastingly increased the femoral mRNA expression of the proinflammatory cytokine interleukin-6 (IL-6) and the osteoclastic markers Cathepsin K and RANKL. Importantly, all sex-specific ELA effects on bone were absent in female mice administered with M. vaccae NCTC (National Collection of Type Cultures) 11659 following ELA exposure. Finally, our clinical data indicate strong associations between ELA and development of an osteopenic/osteoporotic bone phenotype in postmenopausal women undergoing bone diagnostics. Together, our preclinical and clinical findings indicate that i) ELA negatively affects the bone, ii) these effects are specific for female sex, iii) the negative effects of ELA on female bone are associated with transient changes in the composition of the intestinal microbiome followed by long-lasting activation of the immune system and the HPA axis, together setting the stage for a facilitated catabolic bone turnover and development of an osteopenic/osteoporotic bone phenotype, iv) developing immunoregulatory approaches, such as repeated s.c. administrations with immunoregulatory microorganisms, have potential for prevention/treatment of ELA-related bone disorders.
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Left Ventricular Hypertrophy: Roles of Mitochondria CYP1B1 and Melatonergic Pathways in Co-Ordinating Wider Pathophysiology.
Left ventricular hypertrophy (LVH) can be adaptive, as arising from exercise, or pathological, most commonly when driven by hypertension. The pathophysiology of LVH is consistently associated with an increase in cytochrome P450 (CYP)1B1 and mitogen-activated protein kinases (MAPKs) and a decrease in sirtuins and mitochondria functioning. Treatment is usually targeted to hypertension management, although it is widely accepted that treatment outcomes could be improved with cardiomyocyte hypertrophy targeted interventions. The current article reviews the wide, but disparate, bodies of data pertaining to LVH pathoetiology and pathophysiology, proposing a significant role for variations in the N-acetylserotonin (NAS)/melatonin ratio within mitochondria in driving the biological underpinnings of LVH. Heightened levels of mitochondria CYP1B1 drive the 'backward' conversion of melatonin to NAS, resulting in a loss of the co-operative interactions of melatonin and sirtuin-3 within mitochondria. NAS activates the brain-derived neurotrophic factor receptor, TrkB, leading to raised trophic signalling via cyclic adenosine 3',5'-monophosphate (cAMP)-response element binding protein (CREB) and the MAPKs, which are significantly increased in LVH. The gut microbiome may be intimately linked to how stress and depression associate with LVH and hypertension, with gut microbiome derived butyrate, and other histone deacetylase inhibitors, significant modulators of the melatonergic pathways and LVH more generally. This provides a model of LVH that has significant treatment and research implications.
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Multi-omics analysis of the gut microbiome and metabolites associated with the psychoneurological symptom cluster in children with cancer receiving chemotherapy.
BACKGROUND: Children with cancer receiving chemotherapy commonly report a cluster of psychoneurological symptoms (PNS), including pain, fatigue, anxiety, depression, and cognitive dysfunction. The role of the gut microbiome and its functional metabolites in PNS is rarely studied among children with cancer. This study investigated the associations between the gut microbiome-metabolome pathways and PNS in children with cancer across chemotherapy as compared to healthy children. METHODS: A case-control study was conducted. Cancer cases were recruited from Children's Healthcare of Atlanta and healthy controls were recruited via flyers. Participants reported PNS using the Pediatric Patient-Reported Outcomes Measurement Information System. Data for cases were collected pre-cycle two chemotherapy (T0) and post-chemotherapy (T1), whereas data for healthy controls were collected once. Gut microbiome and its metabolites were measured using fecal specimens. Gut microbiome profiling was performed using 16S rRNA V4 sequencing, and metabolome was performed using an untargeted liquid chromatography-mass spectrometry approach. A multi-omics network integration program analyzed microbiome-metabolome pathways of PNS. RESULTS: Cases (n = 21) and controls (n = 14) had mean ages of 13.2 and 13.1 years. For cases at T0, PNS were significantly associated with microbial genera (e.g., Ruminococcus, Megasphaera, and Prevotella), which were linked with carnitine shuttle (p = 0.0003), fatty acid metabolism (p = 0.001) and activation (p = 0.001), and tryptophan metabolism (p = 0.008). Megasphaera, clustered with aspartate and asparagine metabolism (p = 0.034), carnitine shuttle (p = 0.002), and tryptophan (p = 0.019), was associated with PNS for cases at T1. Gut bacteria with potential probiotic functions, along with fatty acid metabolism, tryptophan, and carnitine shuttle, were more clustered in cancer cases than the control network and this linkage with PNS needs further studies. CONCLUSIONS: Using multi-omics approaches, this study indicated specific microbiome-metabolome pathways linked with PNS in children with cancer across chemotherapy. Due to limitations such as antibiotic use in cancer cases, these findings need to be further confirmed in a larger cohort.
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Gut microbes influence the development of central nervous system disorders through epigenetic inheritance.
Central nervous system (CNS) disorders, such as depression, anxiety, and Alzheimer's disease (AD), affect quality of life of patients and pose significant economic and social burdens worldwide. Due to their obscure and complex pathogeneses, current therapies for these diseases have limited efficacy. Over the past decade, the gut microbiome has been shown to exhibit direct and indirect influences on the structure and function of the CNS, affecting multiple pathological pathways. In addition to the direct interactions between the gut microbiota and CNS, the gut microbiota and their metabolites can regulate epigenetic processes, including DNA methylation, histone modification, and regulation of non-coding RNAs. In this review, we discuss the tripartite relationship among gut microbiota, epigenetic inheritance, and CNS disorders. We suggest that gut microbes and their metabolites influence the pathogenesis of CNS disorders at the epigenetic level, which may inform the development of effective therapeutic strategies for CNS disorders.