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The compositional and functional imbalance of the gut microbiota in CKD linked to disease patterns.
BACKGROUND: The prevalence of chronic kidney disease (CKD) is on the rise, posing a significant public health challenge. Although gut microbiome dysbiosis has been implicated in the impairment of kidney functions, the existence of pathological subtypes-linked differences remains largely unknown. We aimed to characterize the intestinal microbiota in patients with membranous nephropathy (MN), IgA nephropathy (IgAN), minimal change disease (MCD), and ischemic renal injury (IRI) in order to investigate the intricate relationship between intestinal microbiota and CKD across different subtypes. METHODS: We conducted a cross-sectional study involving 94 patients with various pathological patterns of CKD and 54 healthy controls (HCs). The clinical parameters were collected, and stool samples were obtained from each participant. Gut microbial features were analyzed using 16S rRNA sequencing and taxon annotation to compare the HC, CKD, MN, IgAN, MCD, and IRI groups. RESULTS: The CKD subjects exhibited significantly reduced alpha diversity, modified community structures, and disrupted microbial composition and potential functions compared to the control group. The opportunistic pathogen Klebsiella exhibited a significant enrichment in patients with CKD, whereas Akkermansia showed higher abundance in HCs. The study further revealed the presence of heterogeneity in intestinal microbial signatures across diverse CKD pathological types, including MN, IgAN, MCD, and IRI. The depression of the family Lachnospiraceae and the genus Bilophila was prominently observed exclusively in patients with MN, while suppressed Streptococcus was detected only in individuals with MCD, and a remarkable expansion of the genus Escherichia was uniquely found in cases of IRI. The study also encompassed the development of classifiers employing gut microbial diagnostic markers to accurately discriminate between distinct subtypes of CKD. CONCLUSIONS: The dysregulation of gut microbiome was strongly correlated with CKD, exhibiting further specificity towards distinct pathological patterns. Our study emphasizes the significance of considering disease subtypes when assessing the impact of intestinal microbiota on the development, diagnosis, and treatment of CKD.
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Lifestyle Modulation of Xenobiotic Stress: Aerobic Exercise Attenuates Nanoplastic-Associated Neuroendocrine Dysfunction via a Gut-Ovary-Brain Continuum.
Xenobiotic stress can disrupt neuroendocrine function, yet whether a modifiable lifestyle factor can alter internal burden and downstream toxicity remains unclear. Here, adult female zebrafish were exposed to polystyrene nanoplastics (NPs; 80 nm; 1.0 mg/L) for 21 days, with or without moderate aerobic exercise (AE; 12 cm/s, 20 min/day). NPs exposure alone caused significant ovarian accumulation of particle-like structures (TEM), elevated oxidative stress, increased follicular apoptosis (TUNEL), and disrupted reproductive hormones (E2, FSH, LH). It also induced anxiety- and depression-like behaviors in novel tank and shoaling tests, accompanied by elevated cortisol and altered monoamine (NE, 5-HIAA) levels. In contrast, concurrent AE markedly attenuated these effects: it reduced ovarian particle burden, improved antioxidant enzyme activities (SOD, POD), restored ovarian histoarchitecture, and normalized endocrine and neuroendocrine measures. These changes were supported by partial recovery of ovarian (ESR1, cyp19a1a, AMH) and brain (BDNF, TPH2) transcript levels. Gut microbiome profiling revealed that AE counteracted NPs-associated dysbiosis, enriching beneficial taxa, including Akkermansia and Lachnospiraceae_NK4A136_group. Predictive functional inference and correlation analyses linked these microbial shifts to enhanced fatty acid and tryptophan metabolic potential, which correlated with neuroendocrine recovery. Together, these data support a working model in which AE acts as an exposure modifier, coupling host physiology and microbiome-associated metabolic capacity to mitigate NPs-induced neuroendocrine dysfunction via a gut-ovary-brain continuum. Targeted metabolomics and causal microbiota perturbation will be needed to validate specific mediators.
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On the role of corticosterone in behavioral disorders, microbiota composition alteration and neuroimmune response in adult male mice subjected to maternal separation stress.
Experiencing psychosocial adversities in early life such as maternal separation (MS) increases the risk of psychiatric disorders. Immune-inflammatory responses have imperative roles in the pathophysiology of psychiatric disorders. MS relatively changes the composition of intestinal microbiota leading to an overactivation of the hypothalamic-pituitary-adrenal (HPA) axis, and subsequently increases the corticosterone level. In this study, we aimed to evaluate the role of corticosterone in behavioral changes and microbiota modifications in a mouse model of MS afflicted neuroinflammatory response in the hippocampus. For this purpose, 180 min of MS stress was applied to mice at postnatal day (PND) 2-14 followed by behavioral tests including forced swimming test (FST), splash test, open field test (OFT) and elevated plus maze (EPM) at PND 50-52. For evaluating the role of corticosterone, mice were subjected to adrenalectomy. Using real-time RT-PCR, the expression of inflammatory genes was determined in the hippocampus and colon tissues. We found that MS provoked depressive- and anxiety-like behaviors in adult male mice. In addition, MS was able to active a neuroimmune response in the hippocampus, motivate inflammation and histopathologic changes in the colon tissue and modify the composition of gut microbiota as well. Interestingly, our findings showed that adrenalectomy (decline in the corticosterone level), could modulate the above-mentioned negative effects of MS. In conclusion, our results demonstrated that overactivation of HPA axis and the subsequent increased level of corticosterone could act, possibly, as the deleterious effects of MS on behavior, microbiota composition changes and activation of neuroimmune response.
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1-Kestose Prevents Psychiatric-Like Behavior by Enhancing Short-Chain Fatty Acid Production.
Psychiatric disorders such as major depressive disorder are closely linked to the intestinal environment, suggesting intestinal health may contribute to their prevention. Prebiotics, which enhance intestinal health, are promising candidates for preventing psychiatric disorders. 1-Kestose (kestose), a type of prebiotics, has shown potential, but its effects on psychiatric disorders remain unclear. In this study, we investigated whether kestose prevents abnormal behaviors induced by social isolation (SI) stress and which underlies mechanisms of preventive effects. C57BL/6J male mice (3 weeks old) were divided into two groups: individually housed (SI) group and housed five mice per cage (GH) group. Each group received either a normal diet or a kestose diet (5% kestose) for 5 weeks daily until the end of the behavioral testing. Kestose prevented the SI-induced abnormal behaviors including reduced sociality, impaired spatial recognition, and heightened anxiety, which were associated with suppressed microglial activation in the hippocampus. Kestose altered the diversity of gut microbiota and increased the abundance of Bacteroides sartorii. Furthermore, short-chain fatty acids (SCFAs) such as butyric acid, acetic acid, and propionic acid, produced by intestinal microbiota, were increased after kestose supplementation. Positive correlations were observed between B. sartorii abundance and SCFA levels, suggesting that B. sartorii contributes to SCFA production. Notably, both B. sartorii and SCFAs were strongly associated with the abnormal behaviors by SI. These findings suggest that kestose prevents SI-induced abnormal behaviors by modulating gut microbiota, particularly B. sartorii, through an increase of SCFA production. Taken together, kestose could be used as a promising prebiotic intervention for psychiatric disorders.
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Chlorogenic Acid-Gut Microbiota Interactions: New Insights for Alleviating Chronic Diseases and Health Disorders.
Chlorogenic acid (CGA) is a natural polyphenol compound found in coffee, fruits, and vegetables. During digestion, a large proportion of dietary CGA is not absorbed and reaches the colon, where it interacts with the gut microflora. CGA can regulate the gut microflora to increase its diversity and proportion of beneficial microflora; reduce harmful microflora; induce changes in gut microflora-derived metabolites, such as short-chain fatty acids, indole compounds, and hydroxycinnamic acid; and indirectly regulate host immunity, gut barrier function, and metabolic homeostasis. It can be degraded into colonic metabolites, such as caffeic and quinic acids, which accumulate in the body and modulate a number of biological activities. Herein, we review the interactions of CGA with the gut microbiota. The progression of chronic diseases and health disorders is closely linked to imbalances in the gut microbiota. Therefore, we focus on the role of the gut microbiota as a mediator to enhance the therapeutic potential of CGA in various chronic diseases and health disorders, including nonalcoholic fatty liver disease, obesity, intestinal diseases, diabetes mellitus, nephropathy, cognitive impairment, and depression-like behavior.
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IMAGINE Network's Mind And Gut Interactions Cohort (MAGIC) Study: a protocol for a prospective observational multicentre cohort study in inflammatory bowel disease and irritable bowel syndrome.
INTRODUCTION: Gut microbiome and diet may be important in irritable bowel syndrome (IBS), inflammatory bowel disease (IBD) and comorbid psychiatric conditions, but the mechanisms are unclear. We will create a large cohort of patients with IBS, IBD and healthy controls, and follow them over time, collecting dietary and mental health information and biological samples, to assess their gastrointestinal (GI) and psychological symptoms in association with their diet, gut microbiome and metabolome. METHODS AND ANALYSIS: This 5-year observational prospective cohort study is recruiting 8000 participants from 15 Canadian centres. Persons with IBS who are 13 years of age and older or IBD ≥5 years will be recruited. Healthy controls will be recruited from the general public and from friends or relatives of those with IBD or IBS who do not have GI symptoms. Participants answer surveys and provide blood, urine and stool samples annually. Surveys assess disease activity, quality of life, physical pain, lifestyle factors, psychological status and diet. The main outcomes evaluated will be the association between the diet, inflammatory, genetic, microbiome and metabolomic profiles in those with IBD and IBS compared with healthy controls using multivariate logistic regression. We will also compare these profiles in those with active versus quiescent disease and those with and without psychological comorbidity. ETHICS AND DISSEMINATION: Approval has been obtained from the institutional review boards of all centres taking part in the study. We will develop evidence-based knowledge translation initiatives for patients, clinicians and policymakers to disseminate results to relevant stakeholders.Trial registration number: NCT03131414.
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The gut-organ axis: Clinical aspects and immune mechanisms.
The gut-brain axis exemplifies the bidirectional connection between the intestines and the brain, as evidenced by the impact of severe stress on gastrointestinal symptoms including abdominal pain and diarrhea, and conversely, the influence of abdominal discomfort on mood. Clinical observations support the notion of the gut-brain connection, including an increased prevalence of inflammatory bowel disease (IBD) in patients with depression and anxiety, as well as the association of changes in the gut microbiota with neurological disorders such as multiple sclerosis, Parkinson's disease, stroke and Alzheimer's disease. The gut and brain communicate via complex mechanisms involving inflammatory cytokines, immune cells, autonomic nerves, and gut microbiota, which contribute to the pathogenesis in certain gut and brain diseases. Two primary pathways mediate the bidirectional information exchange between the intestinal tract and the brain: signal transduction through bloodstream factors, such as bacterial metabolites and inflammatory cytokines, and neural pathways, such as neurotransmitters and inflammatory cytokines within the autonomic nervous system through the interaction between the nerve cells and beyond. In recent years, the basic mechanisms of the pathophysiology of the gut-brain axis have been gradually elucidated. Beyond the gut-brain interaction, emerging evidence suggests the influence of the gut extends to other organs, such as the liver and lungs, through intricate inter-organ communication pathways. An increasing number of reports on this clinical and basic cross-organ interactions underscore the potential for better understanding and novel therapeutic strategies targeting inter-organs networks. Further clarification of interactions between multiorgans premises transformative insights into cross-organ therapeutic strategies.
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Differential effects of different diets on depressive-like phenotypes in C57BL/JJmsSLc mice.
Identical mouse models tested using the same protocols in different laboratories can produce inconsistent results. Indeed, little information is available regarding suitable diets for mouse models of disease in the field of neuroscience. Thus, neuroscientists often select experimental diets based on personal judgment. Recent studies have reported a strong interaction between depression and gut microbiota. Furthermore, diets can impact the composition of the microbiota. To confirm whether diet influences the phenotype and gut microbiota of depressive mice, we examined the effects of two widely used commercial diets, non-purified (CRF-1) and semi-purified (AIN-93 G) commercial diets on behavior, plasma levels of corticosterone, and cecum microbiota at 1 and 5 weeks after restraint in repeatedly restrained mice. Exposure to repeated stress induced similar depression-like phenotypes 1 week after stress in CRF-1 and AIN-93 G fed mice. However, mice fed the AIN-93 G diet showed greater vulnerability than the others 5 weeks after restraint. The Firmicutes to Bacteroidetes ratio and α-diversity were lower in the cecum at 5 weeks after stress in mice fed the AIN-93 G diet compared to 1 week after stress in mice fed the AIN-93 G diet. These data suggest that diet type affects stress sensitivity via different gut microbiota and that diet selection is important in neuroscience research and data reproducibility.
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Intestinal microbiome-gut-brain axis and irritable bowel syndrome.
Psychological comorbidity is highly present in irritable bowel syndrome (IBS). Recent research points to a role of intestinal microbiota in visceral hypersensitivity, anxiety, and depression. Increased disease reactivity to psychological stress has been described too. A few clinical studies have attempted to identify features of dysbiosis in IBS. While animal studies revealed strong associations between stress and gut microbiota, studies in humans are rare. This review covers the most important studies on intestinal microbial correlates of psychological and clinical features in IBS, including stress, anxiety, and depression.
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The role of gut microbiota in shaping and modulating dietary preferences in neurological diseases: implications for microbiota-targeted interventions.
A high percentage of patients with neurological diseases have significant dietary preference abnormalities (such as picky eating and texture sensitivity). Studies show Gut Microbiota (GM) mediates dietary preferences via the microbiota-gut-brain axis (MGBA), such as depression-related appetite changes linked to gut flora imbalance. GM directly or indirectly regulates dietary behavior through the vagal-mediated gut-brain signaling pathway. On the one hand, gut bacterial metabolites (such as butyrate) can directly activate vagal afferents, which project signals through the nucleus of the solitary tract (NTS) to the hypothalamic feeding center to enhance the craving for high-energy foods. The 5-hydroxytryptamine (5-HT) axis of tryptophan metabolism is also involved. On the other hand, gut microbes modulate the efficiency of tryptophan conversion to 5-HT, which in turn affects the limbic reward circuit and alters the emotion-dependent choice of specific foods, such as carbohydrate preference in depressed patients. In addition, enteroendocrine cells sense bacterial products or metabolites in the gut and regulate the activity of the vagus nerve by releasing neurotransmitters or gut hormones. These metabolites can also activate immune cells in the gut and release cytokines, which further affect the activity of the vagus nerve and indirectly regulate brain function. At the same time, change in GM will affect the integrity of the intestinal barrier, which in turn affects the function of the vagus nerve. MGBA shows promise as a target to regulate dietary preferences in neurological diseases, aiding disease management.