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No distinct microbiome signature of irritable bowel syndrome found in a Swedish random population.
OBJECTIVE: The ethiopathogenesis of irritable bowel syndrome (IBS) is unknown. While a link to the gut microbiome is postulated, the heterogeneity of the healthy gut makes it difficult to draw definitive conclusions. We aimed to describe the faecal and mucosa-associated microbiome (MAM) and health correlates on a community cohort of healthy and IBS individuals with no colonoscopic findings. DESIGN: The PopCol study recruited a random sample of 3556 adults; 745 underwent colonoscopy. IBS was defined by Rome IV criteria and organic disease excluded. 16S rRNA gene sequencing was conducted on sigmoid biopsy samples from 376 representative individuals (63 IBS cases) and faecal samples from 185 individuals (32 IBS cases). RESULTS: While sigmoid MAM was dominated by Lachnospiraceae, faeces presented a higher relative abundance of Ruminococcaceae. Microbial richness in MAM was linearly correlated to that in faeces from the same individual (R²=0.255, p<3E-11) as was diversity (R²=0.06, p=0.0022). MAM diversity decreased with increasing body mass index (BMI; Pearson's r=-0.1, p=0.08) and poorer self-rated health (r=-0.15, p=0.007), but no other health correlates. Faecal microbiome diversity was correlated to stool consistency (r=-0.16, p=0.043). Several taxonomic groups were correlated to age, BMI, depression and self-reported health, including Coprococcus catus associated with lower levels of depression (r=-0.003, p=0.00017). The degree of heterogeneity observed between IBS patients is higher than that observed between healthy individuals. CONCLUSIONS: No distinct microbial signature was observed in IBS. Individuals presenting with low self-rated health or high BMI have lower gut microbiome richness.
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The microbiota-gut-brain axis participates in chronic cerebral hypoperfusion by disrupting the metabolism of short-chain fatty acids.
BACKGROUND: Chronic cerebral hypoperfusion (CCH) underlies secondary brain injury following certain metabolic disorders and central nervous system (CNS) diseases. Dysregulation of the microbiota-gut-brain axis can exacerbate various CNS disorders through aberrantly expressed metabolites such as short-chain fatty acids (SCFAs). Yet, its relationship with CCH remains to be demonstrated. And if so, it is of interest to explore whether restoring gut microbiota to maintain SCFA metabolism could protect against CCH. RESULTS: Rats subjected to bilateral common carotid artery occlusion (BCCAO) as a model of CCH exhibited cognitive impairment, depressive-like behaviors, decreased gut motility, and compromised gut barrier functions. The 16S ribosomal RNA gene sequencing revealed an abnormal gut microbiota profile and decreased relative abundance of some representative SCFA producers, with the decreased hippocampal SCFAs as the further evidence. Using fecal microbiota transplantation (FMT), rats recolonized with a balanced gut microbiome acquired a higher level of hippocampal SCFAs, as well as decreased neuroinflammation when exposed to lipopolysaccharide. Healthy FMT promoted gut motility and gut barrier functions, and improved cognitive decline and depressive-like behaviors by inhibiting hippocampal neuronal apoptosis in BCCAO rats. Long-term SCFA supplementation further confirmed its neuroprotective effect in terms of relieving inflammatory response and hippocampal neuronal apoptosis following BCCAO. CONCLUSION: Our results demonstrate that modulating the gut microbiome via FMT can ameliorate BCCAO-induced gut dysbiosis, cognitive decline, and depressive-like behaviors, possibly by enhancing the relative abundance of SCFA-producing floras and subsequently increasing SCFA levels. Video abstract.
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Wastewater-based human gut microbiome surveillance links microbial signatures to population health in Ohio communities.
Wastewater-based epidemiology (WBE) has been widely used to track infectious diseases, yet its potential for population-level gut microbiome surveillance and broader public health assessment remains limited. Here, we present a multi-city study in Ohio, USA, demonstrating how sewage-derived human gut microbiome profiles can be leveraged to infer community health patterns. In this retrospective cross-sectional study, influent wastewater samples were collected from eight Ohio cities (May - June 2022). Community-level gut bacterial profiles were characterized and integrated with publicly available health, lifestyle, socioeconomic, and demographic data using geospatial analysis. Bioinformatic processing and multivariate statistical approaches, including principal component analysis and multiple linear regressions, were used to examine associations between microbial features and population health indicators. Distinct microbial signatures were observed across cities, including variation in clinically relevant taxa such as Bacteroidota, Desulfobacterota, Verrucomicrobiota, Akkermansia, Desulfovibrio, and Streptococcus. Several microbial features, including Firmicutes, Desulfovibrio, Acetobacterium, and alpha diversity, were significantly associated with indicators of chronic disease burden and health-related factors, including smoking, obesity, unemployment, and minority status. Notably, several microbial variables demonstrated statistical associations with multiple community health metrics (e.g., hypertension, high cholesterol, asthma, obesity, smoking, depression, and unemployment), and rural communities generally exhibited higher adverse health burdens alongside distinct microbiome profiles. These findings highlight the feasibility of integrating wastewater-based gut microbiome data with demographic and health indicators to evaluate community health disparities. This study expands the scope of WBE beyond infectious disease monitoring and supports its application in informing targeted and equitable public health interventions.
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A pathophysiologic framework for the overlap of disorders of gut-brain interaction and the role of the gut microbiome.
The International Rome Committee defines Disorders of Gut-Brain Interactions (DGBI) based upon distinct combinations of chronic and/or recurrent unexplained gastrointestinal symptoms. Yet patients often experience overlapping DGBI. Patients with DGBI frequently also suffer from extraintestinal symptoms, including fatigue, sleep disturbances, anxiety, and depression. Patients with overlapping DGBI typically experience more severe GI symptoms and increased psychosocial burden. Concerning the pathophysiology, DGBI are associated with disruptions in gut motility, function of the brain and enteric neurons, immune function, and genetic markers, with recent findings revealing gut microbiome alterations linked to these mechanisms of DGBI. Emerging evidence summarized in this review suggests that the microbiome influences various established disease mechanisms of different DGBI groups. Overall, changes in the gastrointestinal microbiome do not seem to be linked to a specific DGBI subgroup but may play a key role in the manifestation of different DGBI and, subsequently, overlap of DGBI. Understanding these shared mechanisms and the role of the gastrointestinal microbiome, particularly for overlapping DGBI, might aid in developing more precise diagnostic criteria and treatment strategies while developing personalized interventions that target specific mechanisms to improve patient outcomes.
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Decoding the role of the gut microbiome in gut-brain axis, stress-resilience, or stress-susceptibility: A review.
Increased exposure to stress is associated with stress-related disorders, including depression, anxiety, and neurodegenerative conditions. However, susceptibility to stress is not seen in every individual exposed to stress, and many of them exhibit resilience. Thus, developing resilience to stress could be a big breakthrough in stress-related disorders, with the potential to replace or act as an alternative to the available therapies. In this article, we have focused on the recent advancements in gut microbiome research and the potential role of the gut-brain axis (GBA) in developing resilience or susceptibility to stress. There might be a complex interaction between the autonomic nervous system (ANS), immune system, endocrine system, microbial metabolites, and bioactive lipids like short-chain fatty acids (SCFAs), neurotransmitters, and their metabolites that regulates the communication between the gut microbiota and the brain. High fiber intake, prebiotics, probiotics, plant supplements, and fecal microbiome transplant (FMT) could be beneficial against gut dysbiosis-associated brain disorders. These could promote the growth of SCFA-producing bacteria, thereby enhancing the gut barrier and reducing the gut inflammatory response, increase the expression of the claudin-2 protein associated with the gut barrier, and maintain the blood-brain barrier integrity by promoting the expression of tight junction proteins such as claudin-5. Their neuroprotective effects might also be related to enhancing the expression of brain-derived neurotrophic factor (BDNF) and glucagon-like peptide (GLP-1). Further investigations are needed in the field of the gut microbiome for the elucidation of the mechanisms by which gut dysbiosis contributes to the pathophysiology of neuropsychiatric disorders.
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Microbiome and Metabolome Variation as Indicator of Social Stress in Female Prairie Voles.
Social isolation is detrimental to the health of social mammals inducing neurochemical and hormonal changes related to depression and anxiety, as well as impairments of cardiovascular and immune functioning. Likewise, perceptions of loneliness are increasingly recognized as detrimental to human psychological well-being, cognitive functioning, and physical health. Few studies, however, have examined the impact of social isolation on the intestinal microbiome and metabolome. To better understand the impact of social isolation on these systems, intestinal microbiota, and the systemic impact via the gut-brain axis, we employed prairie voles. Physiological stress on female prairie voles (n = 22) either with a same-sex sibling (n = 11) or in isolation (n = 11) for four weeks demonstrated behavioral indicators of increased anxiety and depression in isolated voles (p ≤ 0.01). Bacterial DNA from fecal and colon samples, collected at five time points (T0-4), were sequenced for all nine hypervariable regions of the 16S rRNA gene. Microbiome analyses revealed several differences in gut communities of paired and isolated voles with greater differences at T4. Notably, several taxa associated with host health including Anaerostipes and Lactobacillaceae were more prevalent in paired voles, whereas several taxa associated with known pathogens (e.g., Staphylococcaceae and Enterococcus) or disease were elevated in isolated animals. Similarly, metabolome analyses suggested isolated voles, when compared to paired animals, exhibited differences in metabolites associated with diabetes and colitis. These findings further contribute to our understanding of the harmful effects of social isolation, which cause perturbations in the gut microbiome and serum metabolites.
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An empirically derived method for measuring human gut microbiome alpha diversity: Demonstrated utility in predicting health-related outcomes among a human clinical sample.
The human gut microbiome has emerged as a potential key factor involved in the manifestation of physical and mental health. Despite an explosion of cross-disciplinary interest in researching the gut microbiome, there remains to be a gold-standard method for operationalizing gut microbiome alpha diversity. Given researchers' interest in examining the relationships among gut microbiome alpha diversity and health-related outcomes of interest, a way of operationalizing the microbiome that yields a numeric value, which could be used in common statistical approaches, is needed. Thus, the current study aims to provide methodological guidance for how to operationalize microbiome alpha diversity. Findings suggest that alpha diversity of the human gut microbiome is comprised of two sub-constructs (richness and evenness), and we propose a step-by-step method of creating alpha diversity composite measures based on this key insight. Finally, we demonstrate that our empirically derived richness and evenness composite measures are significantly associated with health-related variables of interest (alcohol use, symptoms of depression) among a human clinical sample.
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A Diet Enriched with Lacticaseibacillus rhamnosus HN001 and Milk Fat Globule Membrane Alters the Gut Microbiota and Decreases Amygdala GABA a Receptor Expression in Stress-Sensitive Rats.
Brain signalling pathways involved in subclinical anxiety and depressed mood can be modulated via the gut brain axis (GBA), providing the potential for diet and dietary components to affect mood. We investigated behavioural, physiological and gut microbiome responses to the Lacticaseibacillus rhamnosus strain HN001 (LactoB HN001™), which has been shown to reduce postpartum anxiety and depression, and a milk fat globule membrane-enriched product, Lipid 70 (SurestartTM MFGM Lipid 70), which has been implicated in memory in stress-susceptible Wistar Kyoto rats. We examined behaviour in the open field, elevated plus maze and novel object recognition tests in conjunction with the expression of host genes in neuro-signalling pathways, and we also assessed brain lipidomics. Treatment-induced alterations in the caecal microbiome and short-chain fatty acid (SCFA) profiles were also assessed. Neither ingredient induced behavioural changes or altered the brain lipidome (separately or when combined). However, with regard to brain gene expression, the L. rhamnosus HN001 + Lipid 70 combination produced a synergistic effect, reducing GABAA subunit expression in the amygdala (Gabre, Gat3, Gabrg1) and hippocampus (Gabrd). Treatment with L. rhamnosus HN001 alone altered expression of the metabotropic glutamate receptor (Grm4) in the amygdala but produced only minor changes in gut microbiota composition. In contrast, Lipid 70 alone did not alter brain gene expression but produced a significant shift in the gut microbiota profile. Under the conditions used, there was no observed effect on rat behaviour for the ingredient combination. However, the enhancement of brain gene expression by L. rhamnosus HN001 + Lipid 70 implicates synergistic actions on region-specific neural pathways associated with fear, anxiety, depression and memory. A significant shift in the gut microbiota profile also occurred that was mainly attributable to Lipid 70.
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A Gut Microbial Metabolite Alleviates Stress-Induced Neurobehavioral Dysfunction in an Alzheimer's Disease Model.
Chronic psychological stress is a known risk factor for neurodegenerative disorders like Alzheimer's disease (AD), but its role in AD neuropathology remains unclear. Using the water-avoidance stress model in the APP/PS1 preclinical mouse model of AD, we investigate how chronic stress exacerbates neurobehavioral dysfunction and cognitive impairment and explore the neuroprotective potential of indole-3-propionate (IPA), a microbiome-derived metabolite, in mitigating these effects. Our findings show that psychological stress leads to depression- and anxiety-like behaviors, as indicated by reduced grooming and exploration behaviors; however, these effects are ameliorated by IPA supplementation. Stress also disrupts the gut microbiome and promotes intestinal inflammation. While IPA does not significantly alter microbiome composition, it mitigates inflammation by normalizing IL-17a and TGF-β gene expression and reducing TNF-⍺ and IL-6 protein levels. Although stress has a limited effect on hippocampal inflammation, IPA suppresses low-grade neuroinflammation by downregulating IL-1β, TNF-⍺, IL-6, and MCP-1 protein levels. Additionally, IPA treatment tends to reduce hippocampal amyloid-β plaques. These findings highlight the detrimental effects of chronic psychosocial stress on AD pathology and suggest that IPA may confer neuroprotection through the gut-immune-brain axis, supporting the therapeutic potential of microbial metabolites in mitigating cognitive decline.
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Gut microbiota: An intermediary between metabolic syndrome and cognitive deficits in schizophrenia.
Gut microbiome interacts with the central nervous system tract through the gut-brain axis. Such communication involves neuronal, endocrine, and immunological mechanisms, which allows for the microbiota to affect and respond to various behaviors and psychiatric conditions. In addition, the use of atypical antipsychotic drugs (AAPDs) may interact with and even change the abundance of microbiome to potentially cause adverse effects or aggravate the disorders inherent in the disease. The regulate effects of gut microbiome has been described in several psychiatric disorders including anxiety and depression, but only a few reports have discussed the role of microbiota in AAPDs-induced Metabolic syndrome (MetS) and cognitive disorders. The following review systematically summarizes current knowledge about the gut microbiota in behavior and psychiatric illness, with the emphasis of an important role of the microbiome in the metabolism of schizophrenia and the potential for AAPDs to change the gut microbiota to promote adverse events. Prebiotics and probiotics are microbiota-management tools with documented efficacy for metabolic disturbances and cognitive deficits. Novel therapies for targeting microbiota for alleviating AAPDs-induced adverse effects are also under fast development.