155. Dietary prebiotics increase Bifidobacterium spp. and Lactobacillus spp. in the gut and promote stress resistance (original) (raw)
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Probiotics Affect One-Carbon Metabolites and Catecholamines in a Genetic Rat Model of Depression
Molecular nutrition & food research, 2018
Probiotics may influence one-carbon (C1) metabolism, neurotransmitters, liver function markers, or behavior. Male adult Flinders Sensitive Line rats (model of depression, FSL; n = 22) received Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 (10or 10colony-forming units/d) or vehicle for 10 weeks. The controls, Flinders Resistant Line rats (FRL, n = 8), only received vehicle. C1-related metabolites were measured in plasma, urine, and different tissues. Monoamine concentrations were measured in plasma, hippocampus, and prefrontal cortex. Vehicle-treated FSL rats had higher plasma concentrations of betaine, choline, and dimethylglycine, but lower plasma homocysteine and liver S-adenosylmethionine (SAM) than FRLs. FSL rats receiving high-dose probiotics had lower plasma betaine and higher liver SAM compared to vehicle-treated FSL rats. FSLs had higher concentrations of norepinephrine, dopamine, and serotonin than FRLs across various brain regions. Probiotics decreased pl...
Scientific Reports, 2015
Since studies on stress processing during visceral inflammation are lacking, we investigated the effects of experimental colitis as well as psychological stress on neurochemical and neuroendocrine changes as well as behaviour in mice. Dextran sulfate sodium (DSS)-induced colitis and water avoidance stress (WAS) were used as mouse models of colitis and mild psychological stress, respectively. We measured WAS-associated behaviour, gene expression and proinflammatory cytokine levels within the amygdala, hippocampus and hypothalamus as well as plasma levels of cytokines and corticosterone in male C57BL/6N mice. Animals with DSS-induced colitis presented with prolonged immobility during the WAS session, which was associated with brain regiondependent alterations of neuropeptide Y (NPY), NPY receptor Y1, corticotropin-releasing hormone (CRH), CRH receptor 1, brain-derived neurotrophic factor and glucocorticoid receptor gene expression. Furthermore, the combination of DSS and WAS increased interleukin-6 and growth regulated oncogene-α levels in the brain. Altered gut-brain signalling in the course of DSS-induced colitis is thought to cause the observed distinct gene expression changes in the limbic system and the aberrant molecular and behavioural stress responses. These findings provide new insights into the effects of stress during IBD.
Frontiers in Pharmacology
Stress is a physiological consequence of the body to adversity. The gut–brain axis and probiotics are gaining interest to provide better treatment for stress and other neurological disorders. Probiotic (Lactobacillus fermentum NMCC-14 and Bacillus clausii, 1010 colony-forming unit/day/animal, per oral) effects were investigated in acute (up to day 7) and subacute (days 8–14) restraint-stressed and normal mice through behavioral paradigms (elevated plus maze: EPM, light dark box/dark light box: LDB, and open field test: OFT). Time spent in the open arms of the EPM, time spent in the light compartment of the LDB, and movable time and time spent in the center of the OFT were significantly (p ≤ 0.05, n = 5) increased in probiotic-treated restraint-stressed mice. Enzyme-linked immunoassay determined blood cortisol and adrenocorticotropic hormone (ACTH) levels, which were reduced significantly (p < 0.05, n = 5) in probiotic-treated restraint-stressed mice. Hematoxylin and eosin-stained...
A Link Between Gut Microbes & Depression: Microbial Activation of the Human Kynurenine Pathway
2018
Our gut microbiota is involved in human development, nutrition, and the pathogenesis of gut disorders, but has more recently been implicated as a possible mechanism in the pathophysiology of several brain disorders, including disorders of mood and affect, such as depression. Researchers have referred to this dynamic, bidirectional signaling pathway between the gut and the brain as the "gut-brain axis." However, most research on this axis has been limited to rodent studies, and there has been little insight into the mechanism behind it. I propose that the kynurenine pathway, where tryptophan is converted to kynurenine, is a compelling mechanism mediating the gut microbiota's influence on depression. Kynurenine is a metabolite associated with depression, and this pathway has been shown to be manipulated through probiotic (Lactobacillus reuteri) consumption. I propose to study a probiotic intervention in humans, which would assess tryptophan metabolism along the kynurenine pathway by measuring metabolites downstream of this pathway. Urine, feces and blood samples would be collected from two groups, control and probiotic treatment, on day zero and day thirty. Colonic biopsies would be obtained on day thirty, and various analyses would be run to measure metabolite concentrations from the collected samples. The results from this study will help clarify a mechanistic connection between gut microbes and depression via the kynurenine pathway. Additionally, findings could indicate that a probiotic intervention has the ability to influence depressive behavior via a two-pronged approach originating from the kynurenine pathway.
Pharmaceutical Sciences
Background: There is a well-documented cross-talk between the gut and brain. Evidence is accumulating to suggest beneficial effects of psychobiotics [prebiotics, probiotics or synbiotics] on psychological distress in disease states. However, their role in healthy status remains relatively unclear. Objectives: The present study was aimed to clarify if psychobiotics could influence behavioral responses and physiological stress in healthy rats. Methods: In the present experiment, 28 male Wistar rats were divided into four groups (healthy rats treated by Lactobacillus plantarum (L.plantarum), inulin and their combination (synbiotic) and control group). Then, psychobiotics were administered to the intervention groups for 8 weeks. Behavioral tests (Morris water maze, Elevated plus maze, and Forced swimming test) were performed at the endpoint. Then, serum and brain levels of superoxide dismutase, malondialdehyde, glutathione peroxidase, total antioxidant capacity, brain-derived neurotroph...
Impact of the gut microbiota on the neuroendocrine and behavioural responses to stress in rodents
OCL, 2015
The gastro-intestinal tract hosts a complex microbial ecosystem, the gut microbiota, whose collective genome coding capacity exceeds that of the host genome. The gut microbiota is nowadays regarded as a full organ, likely to contribute to the development of pathologies when its dynamic balance is disrupted (dysbiosis). In the last decade, evidence emerged that the gut microbiota influences brain development and function. In particular, comparisons between germ-free and conventional laboratory rodents showed that the absence of the gut microbiota exacerbates the hypothalamic pituitary adrenal (HPA) system reactivity to stress and alters the anxiety-like behaviour. Furthermore, the dysfunctions observed in germ-free animals can be corrected if the gut microbiota is restored in early life but not in adulthood, suggesting a critical period for microbiota imprinting on the responsiveness to stress. The modes of action are still to be deciphered. They may involve transport of neuroactive bacterial metabolites to the brain through the bloodstream, stimulation of the vagus nerve or of entero-endocrine cells, or modulation of the immune system and, consequently, of the inflammatory status. The discovery that the gut microbiota regulates the neuroendocrine and behavioural responses to stress paves the way for the hypothesis that gut microbiota dysbioses could contribute to the pathophysiology of anxiety-related disorders. In this regard, treatments of anxiety-prone rodent strains with probiotics or antibiotics aimed at modifying their gut microbiota have shown an anxiolytic-like activity. Clinical trials are now needed to know if results obtained in preclinical studies can translate to humans. Keywords: Gut-brain axis / germ-free / probiotic / hypothalamic pituitary adrenal axis / anxiety Résumé-Effet du microbiote intestinal sur les réponses neuroendocrinienne et comportementale au stress. Le tractus gastro-intestinal héberge une communauté microbienne complexe appelée microbiote, dont le potentiel génétique excède celui de l'hôte en richesse et diversité. Le microbiote intestinal est considéré aujourd'hui comme un véritable organe, susceptible de contribuer au développement de pathologies si son équilibre est rompu (on parle alors de dysbiose). Au cours de la dernière décennie, des travaux ont commencé à mettre en évidence que le microbiote intestinal influençait le développement et le fonctionnement du cerveau. En particulier, des comparaisons entre rongeurs axéniques et conventionnels ont montré que l'absence de microbiote intestinal intensifiait la réponse au stress de l'axe corticotrope et modifiait le niveau d'anxiété. Ces anomalies ne peuvent être corrigées que si la restauration du microbiote chez les animaux axéniques intervient avant l'âge adulte. Ceci suggère l'existence d'une période critique du développement au cours de laquelle le microbiote influence la maturation des structures cérébrales impliquées dans la réponse au stress. Les mécanismes d'action ne sont pas encore complètement élucidés. Pourraient intervenir des métabolites microbiens neuro-actifs, atteignant le cerveau par voie sanguine, une stimulation des afférences intestinales du nerf vague, une stimulation des cellules endocrines de la paroi intestinale, ou une modulation du système immunitaire et, par conséquent, du statut inflammatoire de l'organisme. La découverte que le microbiote intestinal régule les réponses neuroendocrinienne et comportementale au stress conduit à l'hypothèse que des dysbioses du microbiote pourraient contribuer à la physiopathologie des troubles anxieux ou des troubles de l'humeur ayant une composante anxieuse. À cet égard, la modulation du microbiote intestinal avec des probiotiques ou des antibiotiques chez des lignées de rongeurs prédisposées à l'anxiété a un effet de type anxiolytique. Des essais cliniques sont maintenant nécessaires pour déterminer si ces résultats précliniques sont transposables à l'Homme.
Steroids, Stress, and the Gut Microbiome-Brain Axis
Journal of neuroendocrinology, 2017
It is becoming well established that the gut microbiome has a profound impact on human health and disease. In this review, we explore how steroids can influence the gut microbiota, and in turn how the gut microbiota can influence hormone levels. Within the context of the gut microbiome-brain axis, we discuss how perturbations in the gut microbiota can alter the stress axis and behavior. In addition, human studies on the possible role of gut microbiota in depression and anxiety are examined. Finally, we present some of the challenges and important questions that need to be addressed by future research in this exciting new area at the intersection of steroids, stress, gut-brain axis and human health. This article is protected by copyright. All rights reserved.
Journal of Clinical and Basic Research, 2023
Background: Psychological stress (PS) disrupts the gut microbiome, accelerates cognitive decline, and causes a predisposition to certain neurodegenerative diseases. This study was designed to test the hypothesis that the administration of probiotics has beneficial effects on the neurohistology and neurochemistry of the hippocampus following exposure to psychological stress (PS). Methods: Thirty-five adult male Wistar rats weighing 180±5g were randomly assigned to seven groups (n=5) comprising the control, acute PS, acute probiotic treatment (probio), acute PS+probio, chronic PS, chronic probio, and chronic PS+probio groups. Acute stress and chronic PS or probio treatment lasted seven and 14 days, respectively. Each animal in the probio groups was fed 10×106 colony-forming units of lactobacillus acidophilus every other day. In contrast, the PS groups were exposed to predator stress for one hour between 7-10 am daily. The treatments lasted for 14 days. Following euthanasia, blood and hippocampal samples were collected for histology, and ELISA-based assays of interleukin-1β (1IL-1β), Tumor Necrosis Factor-α (TNF-α), dopamine, serotonin, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Results: Data analysis reveals that acute and chronic psychological stress significantly depresses hippocampal serotonin and dopamine levels, induces the overexpression of IL-1β and TNF-α, and causes increased lipid peroxidation and impaired antioxidant parameters. The probiotics groups exhibited statistically better results on all parameters assessed, including bringing hippocampal IL-1β and TNF-α levels toward normal. No obvious histoarchitectural damages were observed in any group. Conclusion: Overall, this study suggests that the gut microbiome might play a significant role in hippocampal function as supplementing it mitigates stress-induced perturbations of hippocampal neurochemistry and redox status.