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Auswahl der wissenschaftlichen Literatur zum Thema „Intestinal brain microbiota axis“
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Zeitschriftenartikel zum Thema "Intestinal brain microbiota axis"
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Zamudio Tiburcio, Alvaro, Héctor Bermudez Ruiz, Silverio Alonso Lopez und Pedro Antonio Reyes Lopez. „Breast Cancer and Intestinal Microbiota Transplantation“. Journal of Clinical Research and Clinical Trials 2, Nr. 3 (07.11.2023): 1–8. http://dx.doi.org/10.59657/2837-7184.brs.23.018.
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Breast cancer has been studied relating it to the intestinal microbiota and its own microbiota. Giving a primary role to the dysbiosis that occurs in both the mammary gland and the intestine. Likewise, metabolic processes and immunological eventualities have been considered as determining factors; By the way, many of them are determined by the intestinal microbiota itself, which is given the deserved name of endocrine gland, because it acts at a distance, and it is not only the super-organ or the new organ, but the multiple studies have generated this honorable new consideration. We break down breast cancer, in order to determine the usefulness of the Intestinal Microbiota Transplant and we observe the importance of Resilience in the Intestinal Microbiota. The clinical significance of Dysbiosis, both breast and intestinal, in the genesis of the condition is emphasized and the importance, which it has, is given to Apoptosis. Generally, the pattern of the breast microbiota, in descending order, is: Proteobacteria, Firmicutes, Actinobacteria and Bacteroidetes. The breast microbiota can be used as a potential biomarker. The importance of the different axes that influence the process are analyzed, such as the Gut-microbiota-brain Axis, the breast-brain axis, the cancer-microbiome-gut axis and the cancer-microbiota-immunity axis. It is pointed out how chemo and radiotherapy affect the intestinal microbiota and breast cancer, as well as antibiotics. Finally, the effect of biotics and Fecal Microbiota Transplant are determined.
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Góralczyk-Bińkowska, Aleksandra, Dagmara Szmajda-Krygier und Elżbieta Kozłowska. „The Microbiota–Gut–Brain Axis in Psychiatric Disorders“. International Journal of Molecular Sciences 23, Nr. 19 (24.09.2022): 11245. http://dx.doi.org/10.3390/ijms231911245.
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Modulating the gut microbiome and its influence on human health is the subject of intense research. The gut microbiota could be associated not only with gastroenterological diseases but also with psychiatric disorders. The importance of factors such as stress, mode of delivery, the role of probiotics, circadian clock system, diet, and occupational and environmental exposure in the relationship between the gut microbiota and brain function through bidirectional communication, described as “the microbiome–gut–brain axis”, is especially underlined. In this review, we discuss the link between the intestinal microbiome and the brain and host response involving different pathways between the intestinal microbiota and the nervous system (e.g., neurotransmitters, endocrine system, immunological mechanisms, or bacterial metabolites). We review the microbiota alterations and their results in the development of psychiatric disorders, including major depressive disorder (MDD), schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), and attention-deficit hyperactivity disorder (ADHD).
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Kohl, Hannah M., Andrea R. Castillo und Javier Ochoa-Repáraz. „The Microbiome as a Therapeutic Target for Multiple Sclerosis: Can Genetically Engineered Probiotics Treat the Disease?“ Diseases 8, Nr. 3 (30.08.2020): 33. http://dx.doi.org/10.3390/diseases8030033.
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There is an increasing interest in the intestinal microbiota as a critical regulator of the development and function of the immune, nervous, and endocrine systems. Experimental work in animal models has provided the foundation for clinical studies to investigate associations between microbiota composition and function and human disease, including multiple sclerosis (MS). Initial work done using an animal model of brain inflammation, experimental autoimmune encephalomyelitis (EAE), suggests the existence of a microbiota–gut–brain axis connection in the context of MS, and microbiome sequence analyses reveal increases and decreases of microbial taxa in MS intestines. In this review, we discuss the impact of the intestinal microbiota on the immune system and the role of the microbiome–gut–brain axis in the neuroinflammatory disease MS. We also discuss experimental evidence supporting the hypothesis that modulating the intestinal microbiota through genetically modified probiotics may provide immunomodulatory and protective effects as a novel therapeutic approach to treat this devastating disease.
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Blagonravova, A. S., E. A. Galova, I. Yu Shirokova und D. A. Galova. „The gut-brain axis — clinical study results“. Experimental and Clinical Gastroenterology, Nr. 6 (25.07.2023): 5–13. http://dx.doi.org/10.31146/1682-8658-ecg-214-6-5-13.
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The aim of the study was to investigate the intestinal microbiome in children with autism spectrum disorders (ASD). The study was observational, cohort, comparative. All the patients included in it were divided into 2 groups. The first (comparison group main) group (n=43) consisted of children preschool aged of 1 and 2 health groups; the second (n=38, main group) children with an established diagnosis of ASD. It was stated that children with ASD are characterized by the most frequent (p=0.001) detection of intestinal dysbiosis; the detection of significant disorders in the form of intestinal dysbiosis of 3-4 degrees (p=0.001); a significant decrease in the total bacterial mass of the intestinal microbiota (γ=0.29, p=0.006); a decrease in the representation of the main representatives of the philometabolic nucleus of the microbiota: Lactobacillus (p<0.05); Bifidobacterium (p<0.05); Bacteroides (p<0.05) and a number of individual producers of polyunsaturated fatty acids (0.001<p≤0.050). A negative relationship was found between the integral indicator of autism severity and the representation of typical E.coli (R=0.57; F=4.17; p<0.045). In that way Autism spectrum disorders in preschool children are associated with changes in intestinal biocenosis. The structure of microbiome differed significantly from that typical for healthy children. There is a relationship between the severity of dysbiotic disorders and the severity of cognitive disorders in absent-minded.
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Obrenovich, Mark, und V. Prakash Reddy. „Special Issue: Microbiota–Gut–Brain Axis“. Microorganisms 10, Nr. 2 (28.01.2022): 309. http://dx.doi.org/10.3390/microorganisms10020309.
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Derovs, Aleksejs, Sniedze Laivacuma und Angelika Krumina. „Targeting Microbiota: What Do We Know about It at Present?“ Medicina 55, Nr. 8 (10.08.2019): 459. http://dx.doi.org/10.3390/medicina55080459.
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The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.
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Mohamadkhani, Ashraf. „Gut Microbiota and Fecal Metabolome Perturbation in Children with Autism Spectrum Disorder“. Middle East Journal of Digestive Diseases 10, Nr. 4 (21.07.2018): 205–12. http://dx.doi.org/10.15171/mejdd.2018.112.
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The brain-intestinal axis concept describes the communication between the intestinal microbiota as an ecosystem of a number of dynamic microorganisms and the brain. The composition of the microbial community of the human gut is important for human health by influencing the total metabolomic profile. In children with autism spectrum disorder (ASD), the composition of the fecal microbiota and their metabolic products has a different configuration of the healthy child. An imbalance in the metabolite derived from the microbiota in children with ASD affect brain development and social behavior. In this article, we review recent discoveries about intestinal metabolites derived from microbiota based on high-yield molecular studies in children with ASD as part of the "intestinal brain axis".
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Kharchenko, Yu V., H. I. Titov, D. H. Kryzhanovskyi, M. P. Fedchenko, H. P. Chernenko, V. V. Filipenko und V. A. Miakushko. „Stress and the Gut-Brain Axis“. Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, Nr. 4 (30.08.2022): 137–46. http://dx.doi.org/10.26693/jmbs07.04.137.
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The purpose of the review was to study the effects of stress on the gut microbiota. Results and discussion. The gut microbiota forms a complex microbial community that has a significant impact on human health. The composition of the microbiota varies from person to person, and it changes throughout life. It is known that the microbiome can be altered due to diet, various processes, such as inflammation and/or stress. Like all other areas of medicine, microbiology is constantly growing. The gut microbiota lives in a symbiotic relationship with the human host. It is now believed to interact with almost all human organs, including the central nervous system, in the so-called «gut-brain-microbiome axis». Recently, a growing level of research is showing that microbes play a much bigger role in our lives than previously thought, and can have a myriad of effects on how we behave and think, and even on our mental health. The relationship between the brain and the microbiota is bidirectional and includes endocrine, neuronal, immune, and metabolic pathways. The microbiota interacts with the brain through various mechanisms and mediators, including cytokines, short-chain fatty acids, hormones, and neurotransmitters. According to the hypothalamic-pituitary-adrenocortical axis imbalance theory, hormonal imbalances are closely related to psychiatric illness, anxiety, and stress disorders. Therefore, the gut microbiome is closely related to the development and functioning of this axis. The microbiota can influence neurotransmitter levels in a variety of ways, including the secretion of gamma-aminobutyric acid, norepinephrine, dopamine, and serotonin, and can even regulate serotonin synthesis. These neurotransmitters can influence the hormonal status of the body, and the hormones themselves can influence the formation of the qualitative and quantitative composition of the microbiota. Accordingly, a change in the composition of the intestinal microbiota may be responsible for modifying the hormonal levels of the human body. The endocrine environment in the gut can also be modulated through the neuro-enteroendocrine system. Conclusion. Today, it is known that microbiota changes can be associated with several disorders of the nervous system, such as neuropsychiatric, neurodegenerative and neuroinflammatory processes. Research in recent decades has shown that disorders of the nervous system and mood disorders are associated with changes in the balance of neurotransmitters in the brain. Therefore, understanding the role of microbiota in the development and functioning of the brain is of great importance
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GIURGIU, Gheorghe, und Manole COJOCARU. „Natural Neuroimunomodulation in Coronavirus Infection“. Annals of the Academy of Romanian Scientists Series on Biological Sciences 9, Nr. 2 (2020): 80–87. http://dx.doi.org/10.56082/annalsarscibio.2020.2.80.
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Dysbiosis of the nasopharyngeal microbiome attracts dysbiosis of the intestinal microbiome and activation of the intestinal microbiome-brain axis. If the first sign of the disease is quickly intervened with the modulation of the activity of the microbiome, implicitly of the immune system (neuroimmunomodulation), the appearance of the disease is eliminated. There is the microbiome: buccal, nasal, intestinal, cardiac, cutaneous and even the microbiome in the brain with which Covid-19 interacts. When the evolution is complicated, it is necessary to intervene with drug treatment to support the affected organs. Although there is also renal impairment, no coronaviruses or traces were found in the patients' urine. Knowing that the infection also causes digestive symptoms, coronaviruses have been shown in faeces. It is said that in 1-2% of cases Covid-19 reaches the bloodstream. The microbiome is essential for promoting immune function to prevent and combat disease. Specifically, with regard to viral infections, there must be an adequate immune response to protect the body. The intestinal microbiota with low diversity will consequently lead to a deficient immune function. The microbiota, the intestine and the brain communicate through the microbiota-intestine-brain axis in a bidirectional way. We assume that the Covid-19 virus creates a dysbiosis of the intestinal microbiome. A healthy gut microbiome is crucial in creating an adequate response to coronavirus. A diverse microbiome is a healthy microbiome, which contains many different species that each play a role in immunity and health. The motivation of the project is the study of the influence of the intestinal microbiota in terms of health and the appearance of symptoms in Covid-19 infection. With the help of Deniplant brand natural remedies, the authors have developed several products for autoimmune, metabolic and neurological diseases that act as immunomodulators of the human microbiome.
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Bogdanova, Natalia M., und Kira A. Kravtsova. „INTESTINAL MICROBIOME. EPILEPSY AND THE POSSIBILITY OF EXPANDING ALTERNATIVE THERAPIES“. Medical Scientific Bulletin of Central Chernozemye (Naučno-medicinskij vestnik Centralʹnogo Černozemʹâ) 24, Nr. 3 (11.11.2023): 107–21. http://dx.doi.org/10.18499/1990-472x-2023-24-3-107-121.
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The development of sequencing technology indicates a key regulatory role for the gut microbiota in several neurological disorders, including epilepsy. The microbiota-gut-brain axis refers to the bi-directional communication between the gut and the brain and regulates gut and central nervous system homeostasis through neural networks, neuroendocrine, immune and inflammatory pathways. The present review discusses the relationship between the gut microbiota and epilepsy, possible pathogenic mechanisms of epilepsy in terms of the microbiota-gut-brain axis, and alternative therapies targeting the gut microbiota. A better understanding of the role of the microbiota in the gutbrain axis will help investigate the mechanism, diagnosis, prognosis, and treatment of intractable epilepsy.
Dissertationen zum Thema "Intestinal brain microbiota axis"
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Sundman, Mark H., Nan-kuei Chen, Vignesh Subbian und Ying-hui Chou. „The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease“. ACADEMIC PRESS INC ELSEVIER SCIENCE, 2017. http://hdl.handle.net/10150/626124.
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As head injuries and their sequelae have become an increasingly salient matter of public health, experts in the field have made great progress elucidating the biological processes occurring within the brain at the moment of injury and throughout the recovery thereafter. Given the extraordinary rate at which our collective knowledge of neurotrauma has grown, new insights may be revealed by examining the existing literature across disciplines with a new perspective. This article will aim to expand the scope of this rapidly evolving field of research beyond the confines of the central nervous system (CNS). Specifically, we will examine the extent to which the bidirectional influence of the gut-brain axis modulates the complex biological processes occurring at the time of traumatic brain injury (TBI) and over the days, months, and years that follow. In addition to local enteric signals originating in the gut, it is well accepted that gastrointestinal (GI) physiology is highly regulated by innervation from the CNS. Conversely, emerging data suggests that the function and health of the CNS is modulated by the interaction between 1) neurotransmitters, immune signaling, hormones, and neuropeptides produced in the gut, 2) the composition of the gut microbiota, and 3) integrity of the intestinal wall serving as a barrier to the external environment. Specific to TBI, existing pre-clinical data indicates that head injuries can cause structural and functional damage to the GI tract, but research directly investigating the neuronal consequences of this intestinal damage is lacking. Despite this void, the proposed mechanisms emanating from a damaged gut are closely implicated in the inflammatory processes known to promote neuropathology in the brain following TBI, which suggests the gut-brain axis may be a therapeutic target to reduce the risk of Chronic Traumatic Encephalopathy and other neurodegenerative diseases following TBI. To better appreciate how various peripheral influences are implicated in the health of the CNS following TBI, this paper will also review the secondary biological injury mechanisms and the dynamic pathophysiological response to neurotrauma. Together, this review article will attempt to connect the dots to reveal novel insights into the bidirectional influence of the gut-brain axis and propose a conceptual model relevant to the recovery from TBI and subsequent risk for future neurological conditions.
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Rincel, Marion. „Role of the gut-brain axis in early stress-induced emotional vulnerability“. Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0870/document.
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Les maladies psychiatriques présentent de fortes comorbidités avec des désordres gastrointestinaux, ce qui suggère l’existence de bases physiopathologiques communes. Une littérature abondante démontre que l’adversité précoce (infection, stress) augmente la vulnérabilité aux désordres psychiatriques à l’âge adulte. Chez le rongeur, le modèle de séparation maternelle induit chez la descendance adulte des comportements hyperanxieux associés à une hypersensibilité au stress, ainsi que des dysfonctionnements de la sphère gastrointestinale. De plus, des études récentes rapportent une hyperperméabilité de la barrière intestinale chez les ratons soumis au stress de séparation, un effet conduisant potentiellement à une dysbiose et une perturbation de la communication intestin-cerveau. Le but de ma thèse était donc d’étudier le rôle de l’axe intestin-cerveau dans la mise en place des effets à long terme du stress précoce. Nos travaux récents ont montré que certains effets à long-terme de la séparation maternelle peuvent être atténués par l’exposition des mères à un régime hyperlipidique. Dans un premier temps, nous avons testé les effets du régime hyperlipidique maternel sur le cerveau et l’intestin de ratons soumis à la séparation maternelle. Nos résultats montrent que le régime maternel hyperlipidique protège de l’augmentation de la permeabilité intestinale induite par le stress. Nous avons ensuite testé le rôle causal de la perméabilité intestinale sur les comportements émotionnels à travers une approche pharmacologique et une approche génétique. Nous rapportons 1) que la restauration de la fonction barrière de l’intestin atténue certains effets de la séparation maternelle et 2) qu’une hyperperméabilité intestinale chez des souris transgéniques non soumises à un stress produit des effets similaires à ceux de la séparation maternelle. Enfin, nous avons examiné les effets d’une adversité précoce multifactorielle sur le cerveau et l’intestin (perméabilité et microbiote) chez la descendance adulte mâle et femelle dans un modèle combinant infection prénatale et séparation maternelle. Nos résultats mettent en évidence un effet sexe très marqué sur les phénotypes comportements et intestinaux. D’autres études sont nécessaires pour identifier les mécanismes sous-tendant les effets de la perméabilité et la dysbiose intestinale sur la vulnérabilité émotionnelle associée au stress précoceEarly-life adversity is a main risk factor for psychiatric disorders at adulthood; however the mechanisms underlying the programming effect of stress during development are still unknown. In rodents, chronic maternal separation has long lasting effects in adult offspring, including hyper-anxiety and hyper-responsiveness to a novel stress, along with gastrointestinal dysfunctions. Moreover, recent studies report gut barrier hyper-permeability in rat pups submitted to maternal separation, an effect that could potentially lead to dysbiosis and altered gut-brain communication. Therefore, the aim of my PhD was to unravel the role of the gut-brain axis in the neurobehavioral effects of early-life stress. We recently reported that some neural, behavioral and endocrine alterations associated with maternal separation in rats could be prevented by maternal exposure to a high-fat diet. We first addressed the effects of maternal high-fat diet on brain and gut during development in the maternal separation model. We show that maternal high-fat diet prevents the stress-induced decrease in spine density and altered dendritic morphology in the medial prefrontal cortex. Moreover, maternal high-fat diet also attenuates the exacerbated intestinal permeability associated with maternal separation. To explore a potential causal impact of gut leakiness on brain functions, we then examined the impact of pharmacological and genetic manipulations of intestinal permeability on brain and behavior. We report 1) that restoration of gut barrier function attenuates some of the behavioral alterations associated with maternal separation and 2) that chronic gut leakiness in naive adult transgenic mice recapitulates the effects of maternal separation. Finally, we examined the effects of multifactorial early-life adversity on behavior, gut function and microbiota composition in males and females using a combination of prenatal inflammation and maternal separation in mice. At adulthood, offspring exposed to early adversity displayed sex-specific behavioral (social behavior deficits in males and increased anxiety in females) and intestinal phenotypes. In conclusion, our work demonstrates an impact of gut dysfunctions, in particular gut leakiness, on the emergence of emotional alterations. Further studies are needed to unravel the role of the gut dysbiosis in the expression of the behavioral phenotypes associated with early-life adversity
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Marsilio, Ilaria. „Functional and Molecular Studies of the Crosstalk between Intestinal Microbioma and Enteric Nervous System and Potential Effects on the Gut-Brain Axis“. Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3427312.
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L'interazione fra costituenti della parete intestinale e microflora commensale costituisce il principale artefice del mantenimento della barriera mucosale, della promozione dello sviluppo del tratto gastrointestinale (GI) e della modulazione delle funzioni GI. In questo contesto, giocano un ruolo chiave i recettori Toll-like (TLRs), un sistema di proteine che attivano la risposta immunitaria innata e assicurano l'integrità funzionale e strutturale del SNE. In questo studio sono state caratterizzate le alterazioni strutturali e funzionali del SNE murino indotte da: i) cambiamenti nel segnale dell’immunità innata, mediato dal recettore TLR4, ii) una miscela di fosfolipidi ossidati (OxPAPC), implicati nel blocco del segnale generato dai recettori TLR2 e TLR4 e iii) anomalie nella composizione del microbiota.
Data l’importanza di un corretto segnale TLRs-dipendente nel mantenimento della rete nervosa e del codice neurochimico del SNE, segmenti di ileo provenienti da topi WT e TLR4-/- hanno evidenziato anomalie nell’attività contrattile neuromuscolare associate ad un’eccessiva modulazione inibitoria da NO ed ATP, a sostegno della presenza di un dialogo tra TLR4, SNE e microflora, fondamentale per la modulazione della funzione neuromuscolare. Studi strutturali su preparati di ileo di topi TLR4-/- evidenziano un’alterata architettura del SNE a livello gliale, indicando un coinvolgimento del recettore TLR4 nel mantenimento dell'integrità della rete gliale enterica mediato dalla produzione di ATP e della trasmissione purinergica evidenziano il ruolo di TLR4 nell’omeostasi strutturale e funzionale del SNE. Inoltre, è stato dimostrato che la mancanza del recettore TLR4 determina nell’ippocampo, come a livello del SNE, una compromessa neuroplasticità caratterizzata da alterazioni nella densità neuronale associata a variazioni della distribuzione della rete gliale, a confermare un ruolo fondamentale del segnale TLRs anche a livello centrale.
In parallelo, è stato indagato il ruolo del segnale mediato dai TLRs nell’asse microbiota-TLRs-SNE, tramite la somministrazione in acuto con OxPAPC, inibitore del segnale mediato da entrambi i recettori TLR2 e TLR4, in topi adolescenti (3 ± 1 settimane). Il trattamento con OxPAPC ha causato un’alterazione significativa della risposta neuromuscolare associata a modifiche della rete neuro-gliale del SNE, confermando l’importanza del segnale mediato da tali recettori nell'assicurare l’integrità funzionale e strutturale del SNE durante l'adolescenza. Recenti studi riportano un ruolo primario nel dialogo tra i recettori TLRs e il sistema serotoninergico ed è stato evidenziato come OxPAPC comporti iperesponsività alla serotonina, alterazioni nella distribuzione recettoriale serotoninergica associata a variazioni nel metabolismo del triptofano, a sostegno della presenza di un dialogo tra immunità innata e sistema serotoninergico.
Al fine di approfondire il ruolo dell'asse microbiota-intestino nell’omeostasi del SNE è stato messo a punto un modello animale di deplezione di microbiota intestinale attraverso la somministrazione di 4 antibiotici a topi adolescenti. Tale trattamento ha determinato un fenotipo simil germ-free ed alterazioni della motilità intestinale e dell'integrità della rete neuronale e gliale enterica. Data l’importanza di una corretta composizione del microbiota commensale nel mantenimento del codice neurochimico del SNE che nella produzione di neurotrasmettitori a livello enterico, sono state studiate le vie di neurotrasmissione coinvolte nella sensibilità viscerale. Un’alterata composizione del microbiota intestinale altera la sensibilità viscerale associata anomalie nella risposta neuromuscolare alla serotonina accompagnate da una compromessa rete recettoriale serotoninergica e del metabolismo del triptofano, sottolineando l’importanza di una corretta composizione del microbiota nel mantenimento delle funzioni mediate dal sistema serotoninergico.
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Charton, Elise. „Lait humain vs. préparation pour nourrissons : digestibilité des protéines et impact sur l’axe microbiote-intestin-cerveau“. Electronic Thesis or Diss., Rennes, Agrocampus Ouest, 2023. http://www.theses.fr/2023NSARB368.
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Une majorité de nourrissons reçoivent encore aujourd’hui des préparations pour nourrissons (PPN), fabriquées à base de lait bovin et soumises à de nombreux traitements technologiques. Ces substituts ont pour but de mimer au mieux le lait humain (LH). Cependant, malgré l’évolution des PPNs, des différences persistent entre le LH et les PPNs en termes de composition et structure, et effets sur le développement et la santé à court et long termes du nourrisson et adulte en devenir. L’objectif de ce travail était de comprendre comment la nature de l’alimentation infantile, LH vs. PPN, modulait la digestibilité protéique et, plus globalement, comment elle influençait l’axe microbiote intestin-cerveau. Deux modèles du nourrisson humain ont été utilisés et comparés, le mini-porc Yucatan entre 16 et 21 jours de vie, et un modèle de digestion in vitro dynamique paramétré pour mimer le nourrisson à terme. Les contenus digestifs et tissus ont ensuite été analysés via des approches métagénomique (microbiote), histologique et de perméabilité ex vivo (physiologie intestinale), d’expression génique et de métabolomique ciblée (intestin, cerveau et plasma). Les résultats ont montré que la digestibilité de l’azote total et dans une moindre mesure, celle de certains acides aminés (Lys, Phe, Thr, Val, Ala, Pro et Ser) différaient entre LH et PPN. Les deux modèles de digestion (in vivo et in vitro) étudiés ont conduit à des résultats similaires en termes de déstructuration des aliments et du taux de protéines intactes résiduelles en phase gastrique. Le modèle de digestion in vitro dynamique utilisé ici est donc un bon outil de prédiction de la digestion in vivo. L’axe microbiote-intestin-cerveau et notamment la composition du microbiote, ainsi que le métabolisme du tryptophane, malgré une digestibilité similaire entre aliments, étaient modulés différemment par le LH et la PPN. L’augmentation de la permeabilité intestinale, bien que modérée, était associée à un renforcement du système immunitaire mucosal avec le LH. Ces modifications sont associées à des changements d’expression génique (fonctions barrière et endocrine, récepteurs aux AGV) aux niveaux hypothalamique et striatal, et de profils métaboliques principalement aux niveaux hippocampique et plasmatique. Certains composants présents dans le LH (ex.: oligosaccharides, azote non protéique tel que l’urée, consortium bactérien) et absent dans la PPN peuvent expliquer ces résultats. La supplémentation des PPNs en ces composants bioactifs et/ou la modulation de la fraction protéique pourraient être des leviers pour l’optimisation des PPNsNowadays, a high rate of infants is still being fed infant formulas (IF) based on cow milk and subjected to several technological treatments. These substitutes aim to mimic as close as possible the human milk (HM). Despite of IF improvement, differences still exist between HM and IF in terms of composition and structure, and effects on health in infancy, and later on in adulthood. The objective of this work was to understand how the infant food modulated the dietary nitrogen digestibility and, in overall, how it shaped the microbiota-gut-brain axis. Two infant models were used and compared, the 16 to 21-day-old mini-piglet Yucatan and an in vitro dynamic digestion model parametered with term infant digestive conditions. Digestive contents and tissues were then analyzed using metagenomic (microbiota), histological and ex vivo permeability (intestinal physiology) approaches, gene expression and targeted-metabolomic approaches (intestine, brain and plasma). The results showed that the digestibility of nitrogen and at least extent, that of a few amino acids (Lys, Phe, Thr, Val, Ala, Pro and Ser) were different between HM and IF. The two digestion models (in vivo and in vitro) led to similar observations in terms of meal deconstruction and proteolysis, showing that the in vitro dynamic digestion model is a good proxy of the in vivo digestion regarding digestion kinetics. The microbiota-gut-brain axis, notably regarding the colonic microbial composition and the tryptophan metabolism, which digestibility was similar between infant foods, were differently modulated by HM and IF. The increase of the intestinal permeability, though moderately, was associated with a boost of the intestinal immune system and changes in gene expression (barrier and endocrine functions, volatile fatty acids receptors) at hypothalamic and striatal levels and with changes in hippocampal and plasma metabolomic profiles. Some components present in HM (e.g.: oligosaccharides, non-protein nitrogen such as urea, bacteria consortia) and absent in IF can explain the discrepancies observed. IF-supplementation with these bioactive components and/or with the modulation of the protein profile would be of interest for further investigation
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De, Vadder Filipe. „Détection portale des nutriments et contrôle de l'homéostasie énergétique par l'axe nerveux intestin-cerveau“. Phd thesis, Université Claude Bernard - Lyon I, 2014. http://tel.archives-ouvertes.fr/tel-01058661.
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La production endogène de glucose est une fonction cruciale de l'organisme, permettant de maintenir l'homéostasie glycémique. Alors que la production accrue de glucose par le foie a des effets délétères, la néoglucogenèse intestinale (NGI) exerce des effets bénéfiques sur l'équilibre métabolique de l'organisme. Les régimes hyperprotéiques sont connus pour leurs effets de satiété. Grâce à des travaux physiologiques et moléculaires chez le rat et la souris, nous montrons dans une première partie que l'effet bénéfique des régimes hyperprotéiques passe par une induction de la NGI. Lors de la digestion des protéines alimentaires, des di- et tripeptides sont libérés dans la veine porte. Ces molécules agissent comme des antagonistes des récepteurs μ-opioïdes de la veine porte, initiant un arc réflexe intestin-cerveau induisant la NGI et la satiété. Dans un deuxième temps, nous proposons un modèle rendant compte des effets bénéfiques des régimes riches en fibres, tels que l'amélioration de la sensibilité à l'insuline et l'induction de la dépense énergétique. Les fibres solubles sont fermentées par le microbiote intestinal, produisant des acides gras à chaîne courte (AGCC), acétate, propionate et butyrate, à l'origine des effets métaboliques observés. Nous montrons que le butyrate active directement les gènes de la NGI dans les entérocytes, et que le propionate se lie aux récepteurs FFAR3 dans le système nerveux périportal, initiant un mécanisme de communication entre l'intestin et le cerveau induisant la NGI. De plus, nous montrons que la modification de la composition du microbiote par les fibres alimentaires n'est pas suffisante en soi pour induire les effets bénéfiques en absence de NGI
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Strati, Francesco. „The microbiota-gut-brain axis: characterization of the gut microbiota in neurological disorders“. Doctoral thesis, Università degli studi di Trento, 2017. https://hdl.handle.net/11572/368893.
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The human gut microbiota plays a crucial role in the functioning of the gastrointestinal tract and its alteration can lead to gastrointestinal abnormalities and inflammation. Additionally, the gut microbiota modulates central nervous system (CNS) activities affecting several aspect of host physiology. Motivated by the increasing evidences of the role of the gut microbiota in the complex set of interactions connecting the gut and the CNS, known as gut-brain axis, in this Ph.D. thesis we asked whether the gastrointestinal abnormalities and inflammation commonly associated with neurological disorders such as Rett syndrome (RTT) and Autism could be related to alterations of the bacterial and fungal intestinal microbiota.
First, since only few reports have explored the fungal component of the gut microbiota in health and disease, we characterized the gut mycobiota in a cohort of healthy individuals, in order to reduce the gap of knowledge concerning factors influencing the intestinal microbial communities. Next, we compared the gut microbiota of three cohorts of healthy, RTT and autistic subjects to investigate if these neurological disorders harbour alterations of the gut microbiota. Culture-based and metataxonomics analysis of the faecal fungal populations of healthy volunteers revealed that the gut mycobiota differs in function of individuals’ life stage in a gender-related fashion. Different fungal species were isolated showing phenotypic adaptation to the intestinal environment. High frequency of azoles resistance was also found, with potential clinical significance.
It was further observed that autistic subjects are characterized by a reduced incidence of Bacteroidetes and that Collinsella, Corynebacterium, Dorea and Lactobacillus were the taxa predominating in the gut microbiota of autistic subjects. Constipation has been associated with different bacterial patterns in autistic and neurotypical subjects, with constipated autistic individuals characterized by higher levels of Escherichia/Shigella and Clostridium cluster XVIII than constipated neurotypical subjects. RTT is a neurological disorder caused by loss-of-function mutations of MeCP2 and it is commonly associated with gastrointestinal dysfunctions and constipation. We showed that RTT subjects harbour bacterial and fungal microbiota altered from those of healthy controls, with a reduced microbial richness and dominated by Bifidobacterium, different Clostridia and Candida. The alterations of the gut microbiota observed did not depend on the constipation status of RTT subjects while this microbiota produced altered SCFAs profiles potentially contributing to the constipation itself. Phenotypical and immunological characterizations of faecal fungal isolates from RTT subjects showed Candida parapsilosis as the most abundant species isolated in RTT, genetically unrelated to healthy controls’ isolates and with elevated resistance to azoles. Furthermore these isolates induced high levels of IL-10 suggesting increased tolerance and persistence within the host. Finally, the importance of multiple sequence alignment (MSA) accuracy in microbiome research was investigated comparing three implementations of the widely used NAST algorithm. By now, different implementations of NAST have been developed but no one tested the performances and the accuracy of the MSAs generated with these implementations. We showed that micca, a new bioinformatics pipeline for metataxonomics data improves the quality of NAST alignments by using a fast and memory efficient reimplementation of the NAST algorithm.
7
Strati, Francesco. „The microbiota-gut-brain axis: characterization of the gut microbiota in neurological disorders“. Doctoral thesis, Università degli studi di Trento, 2017. http://hdl.handle.net/10449/38243.
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The human gut microbiota plays a crucial role in the functioning of the gastrointestinal tract and its alteration can lead to gastrointestinal abnormalities and inflammation. Additionally, the gut microbiota modulates central nervous system (CNS) activities affecting several aspect of host physiology. Motivated by the increasing evidences of the role of the gut microbiota in the complex set of interactions connecting the gut and the CNS, known as gut-brain axis, in this Ph.D. thesis we asked whether the gastrointestinal abnormalities and inflammation commonly associated with neurological disorders such as Rett syndrome (RTT) and Autism could be related to alterations of the bacterial and fungal intestinal microbiota.
First, since only few reports have explored the fungal component of the gut microbiota in health and disease, we characterized the gut mycobiota in a cohort of healthy individuals, in order to reduce the gap of knowledge concerning factors influencing the intestinal microbial communities. Next, we compared the gut microbiota of three cohorts of healthy, RTT and autistic subjects to investigate if these neurological disorders harbour alterations of the gut microbiota.
Culture-based and metataxonomics analysis of the faecal fungal populations of healthy volunteers revealed that the gut mycobiota differs in function of individuals’ life stage in a gender-related fashion. Different fungal species were isolated showing phenotypic adaptation to the intestinal environment. High frequency of azoles resistance was also found, with potential clinical significance.
It was further observed that autistic subjects are characterized by a reduced incidence of Bacteroidetes and that Collinsella, Corynebacterium, Dorea and Lactobacillus were the taxa predominating in the gut microbiota of autistic subjects. Constipation has been associated with different bacterial patterns in autistic and neurotypical subjects, with constipated autistic individuals characterized by higher levels of Escherichia/Shigella and Clostridium cluster XVIII than constipated neurotypical subjects.
RTT is a neurological disorder caused by loss-of-function mutations of MeCP2 and it is commonly associated with gastrointestinal dysfunctions and constipation. We showed that RTT subjects harbour bacterial and fungal microbiota altered from those of healthy controls, with a reduced microbial richness and dominated by Bifidobacterium, different Clostridia and Candida. The alterations of the gut microbiota observed did not depend on the constipation status of RTT subjects while this microbiota produced altered SCFAs profiles potentially contributing to the constipation itself.
Phenotypical and immunological characterizations of faecal fungal isolates from RTT subjects showed Candida parapsilosis as the most abundant species isolated in RTT, genetically unrelated to healthy controls’ isolates and with elevated resistance to azoles. Furthermore these isolates induced high levels of IL-10 suggesting increased tolerance and persistence within the host.
Finally, the importance of multiple sequence alignment (MSA) accuracy in microbiome research was investigated comparing three implementations of the widely used NAST algorithm. By now, different implementations of NAST have been developed but no one tested the performances and the accuracy of the MSAs generated with these implementations. We showed that micca, a new bioinformatics pipeline for metataxonomics data improves the quality of NAST alignments by using a fast and memory efficient reimplementation of the NAST algorithm.
8
Strati, Francesco. „The microbiota-gut-brain axis: characterization of the gut microbiota in neurological disorders“. Doctoral thesis, University of Trento, 2017. http://eprints-phd.biblio.unitn.it/1917/1/STRATI_PhD_thesis_R1_2017.01.13.pdf.
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The human gut microbiota plays a crucial role in the functioning of the gastrointestinal tract and its alteration can lead to gastrointestinal abnormalities and inflammation. Additionally, the gut microbiota modulates central nervous system (CNS) activities affecting several aspect of host physiology. Motivated by the increasing evidences of the role of the gut microbiota in the complex set of interactions connecting the gut and the CNS, known as gut-brain axis, in this Ph.D. thesis we asked whether the gastrointestinal abnormalities and inflammation commonly associated with neurological disorders such as Rett syndrome (RTT) and Autism could be related to alterations of the bacterial and fungal intestinal microbiota.
First, since only few reports have explored the fungal component of the gut microbiota in health and disease, we characterized the gut mycobiota in a cohort of healthy individuals, in order to reduce the gap of knowledge concerning factors influencing the intestinal microbial communities. Next, we compared the gut microbiota of three cohorts of healthy, RTT and autistic subjects to investigate if these neurological disorders harbour alterations of the gut microbiota. Culture-based and metataxonomics analysis of the faecal fungal populations of healthy volunteers revealed that the gut mycobiota differs in function of individuals’ life stage in a gender-related fashion. Different fungal species were isolated showing phenotypic adaptation to the intestinal environment. High frequency of azoles resistance was also found, with potential clinical significance.
It was further observed that autistic subjects are characterized by a reduced incidence of Bacteroidetes and that Collinsella, Corynebacterium, Dorea and Lactobacillus were the taxa predominating in the gut microbiota of autistic subjects. Constipation has been associated with different bacterial patterns in autistic and neurotypical subjects, with constipated autistic individuals characterized by higher levels of Escherichia/Shigella and Clostridium cluster XVIII than constipated neurotypical subjects. RTT is a neurological disorder caused by loss-of-function mutations of MeCP2 and it is commonly associated with gastrointestinal dysfunctions and constipation. We showed that RTT subjects harbour bacterial and fungal microbiota altered from those of healthy controls, with a reduced microbial richness and dominated by Bifidobacterium, different Clostridia and Candida. The alterations of the gut microbiota observed did not depend on the constipation status of RTT subjects while this microbiota produced altered SCFAs profiles potentially contributing to the constipation itself. Phenotypical and immunological characterizations of faecal fungal isolates from RTT subjects showed Candida parapsilosis as the most abundant species isolated in RTT, genetically unrelated to healthy controls’ isolates and with elevated resistance to azoles. Furthermore these isolates induced high levels of IL-10 suggesting increased tolerance and persistence within the host. Finally, the importance of multiple sequence alignment (MSA) accuracy in microbiome research was investigated comparing three implementations of the widely used NAST algorithm. By now, different implementations of NAST have been developed but no one tested the performances and the accuracy of the MSAs generated with these implementations. We showed that micca, a new bioinformatics pipeline for metataxonomics data improves the quality of NAST alignments by using a fast and memory efficient reimplementation of the NAST algorithm.
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Altera, Annalisa. „Gut-brain axis: the role of microbiota in gut and brain ageing“. Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1209555.
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In the last decade there has been a growing interest in the reciprocal impact occurring between the gut and the brain and this is well conceptualized in the gut-brain axis notion. The gut-brain axis is the bidirectional communication route between the “little brain” (gut) and the “big brain” (brain). There are several factors that play an important role in this axis but it has become more and more evident that the gut bacteria represent a key component. This has led to the new concept of the microbiota-gut-brain axis, emphasizing the importance of the gut microbiota in this axis. The gut has evolved with bacteria in a symbiotic way and the human gut hosts about 1014 bacterial cells. Researches in the last years have highlighted the importance of the microbiota not only for gut functions but also for the central nervous system (CNS) development, physiology and pathology. However, there are different factors that influence the composition of the gut microbiota (mode of delivery, diet, stress and ageing). In particular, the composition of the gut microbiota changes with ageing: in the adults the majority of taxa are Bacteroidetes and Firmicutes while the elderly has a different composition of the gut microbiota. Some studies have reported a decrease in Bifidobacteria and an increase in Escherichia, Enterobacteriaceae and Clostridium difficile in the elderly. Interestingly, the centenarians apparently have no changes in gut microbiota in comparison to adult, further highlighting the importance of gut bacteria in longevity. Ageing is a physiological process related to the loss of function in different body systems and also associated with a decline in cognitive functions. It has become more and more evident that events taking place in the gut play a major role in the ageing process and in age-related diseases. Faecal microbial transplant (FMT) is a technique that consists in the transfer of gut microbiota from a donor to a recipient (usually via an oral gavage in rodents or colonoscopy in humans) and allows to establish a donor-like microbiota in the gastro-intestinal tract of the recipient. FMT is used to treat recurrent Clostridium difficile infections but there are studies trying to test this technique in the treatment of other pathologies such as irritable bowel syndrome, inflammatory bowel disease and constipation. It is also worth noticing that the
imbalance in the composition of the gut microbiota (dysbiosis) has been associated with a plethora of neurological disorders. In this context FMT is being investigated as a therapeutic option not only for treatment of gut disorders but also for diseases of the CNS. The present thesis illustrates a series of experiments by which we tested the impact of FMT from aged donor mice into young adult recipients. Controls were carried out operating FMT from young adult donor mice to age-matched recipients. Following transplantation, characterization of the microbiota and metabolomics profiles along with a series of cognitive and behavioural tests were carried out. Label-free quantitative proteomics was employed to evaluate protein expression in the hippocampus and gut after the transplant.
In addition, in the attempt to elucidate the mechanisms underlying microbiota-host interactions within the framework of the gut-brain axis, we worked on setting up a procedure to tracking down and visualize bacterial metabolites (such as peptides and lipids) that are thought to play a role acting as signaling molecules. To this end, we used copper-catalysed azide-alkyne cycloaddition (CuAAC) click chemistry, a biorthogonal reaction of widespread utility throughout medical chemistry and chemical biology. We sought to optimize click-based protocols to detect the production of lipids in gut-bacteria to track the metabolism of active bacterial cells. This technique use click chemistry to stain synthetic (e.g., noncanonical) precursors incorporated into bacterial cell biomass. After incorporation, the artificial molecules can be fluorescently detected via azide-alkyne reaction and visualized by confocal microscopy.
FMT from aged mice into adult recipients affected spatial learning and memory while we did not observe effects on locomotion and explorative behaviour. Alongside, there was an alteration in the expression of proteins related to synaptic plasticity and neurotransmission in the hippocampus which was not observed in controls. FMT from aged into young adult mice did not induce a significant increase in glial fibrillary acidic protein expression in hippocampal astrocytes suggesting the lack of an overt neuroinflammatory response. On the other hand, a significant increase in the expression of F4/80, a typical trait of the ageing brain, was observed in microglial cells resident in the fimbria. Gut permeability and levels of systemic and local (hippocampus, gut) cytokines were not affected. As regards click chemistry, we used
Bacteroides thetaiotaomicron grown in minimal medium supplemented with palmitic acid alkyne (PAA) and stained this molecule using an azide-containing fluorescent dye. After palmitic acid staining, co-culture experiments were performed to assess the transfer of this bacterial product to eukaryotic cell lines (CaCo2 and SK-N-SH cell lines). The successful transfer to host cells was confirmed by confocal microscopy. Results obtained in FMT experiments highlighted the importance of the gut microbiota on protein expression and functions of CNS. These results support the key role of microbiota in gut-brain axis and it would be of great importance to get more insight into the restoration of a young microbiota in the elderly to try to improve cognitive functions and the quality of life. Click chemistry experiments demonstrate that this technique could be employed to track molecules produced by gut bacteria to unveil their role in host-microbe interactions.
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Gorard, David A. „Intestinal motor function and the brain-gut axis in irritable bowel syndrome“. Thesis, Imperial College London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395770.
Der volle Inhalt der QuelleBücher zum Thema "Intestinal brain microbiota axis"
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Lyte, Mark, und John F. Cryan, Hrsg. Microbial Endocrinology: The Microbiota-Gut-Brain Axis in Health and Disease. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4.
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2
Lyte, Mark, und J. F. Cryan. Microbial endocrinology: The microbiota-gut-brain axis in health and disease. New York: Springer, 2014.
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Petrella, Carla, Giuseppe Nisticò und Robert Nisticò. Gut–brain axis: Physiology and pathology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0007.
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A large body of research has shown the presence of a complex pathway of communication between gut and brain. It is now recognized that, through this pathway, microbiota can influence intestinal homeostasis and modulate brain plasticity in normal and pathological conditions. This chapter provides an overview of preclinical and clinical evidence supporting the possible mechanisms whereby microbiota can influence gastrointestinal function and stress-related behaviour. Since normalization of gut flora can prevent changes in behaviour, the authors further postulate that the gut–brain axis might represent a possible target for pharmacological and dietary strategies aimed at improving intestinal and mental health.
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Evrensel, Alper, und Barış Önen Ünsalver, Hrsg. Gut Microbiota - Brain Axis. IntechOpen, 2018. http://dx.doi.org/10.5772/intechopen.75784.
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Foster, Jane A., und Rochellys Diaz Heijtz. Microbiota-Brain Axis: A Neuroscience Primer. Elsevier Science & Technology Books, 2020.
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Foster, Jane A., und Rochellys Diaz Heijtz. Microbiota-Brain Axis: A Neuroscience Primer. Elsevier Science & Technology, 2020.
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Lyte, Mark, und John F. Cryan. Microbial Endocrinology: The Microbiota-Gut-Brain Axis in Health and Disease. Springer, 2016.
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Stanton, Catherine, und Niall Hyland. Gut-Brain Axis: Dietary, Probiotic, and Prebiotic Interventions on the Microbiota. Elsevier Science & Technology Books, 2016.
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Stanton, Catherine, und Niall Hyland. Gut-Brain Axis: Dietary, Probiotic, and Prebiotic Interventions on the Microbiota. Elsevier Science & Technology Books, 2016.
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Stanton, Catherine, und Niall Hyland. Gut-Brain Axis: Dietary, Probiotic, and Prebiotic Interventions on the Microbiota. Elsevier Science & Technology Books, 2023.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Intestinal brain microbiota axis"
1
Evrensel, Alper, und Mehmet Emin Ceylan. „Gut-Microbiota-Brain Axis and Depression“. In Understanding Depression, 197–207. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6580-4_17.
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2
Khan, Mahejibin, und Nidhi Sori. „Diet-Gut Microbiota-Brain Axis and IgE-Mediated Food Allergy“. In Microbiome-Gut-Brain Axis, 153–68. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-1626-6_6.
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Gareau, Mélanie G. „Microbiota-Gut-Brain Axis and Cognitive Function“. In Advances in Experimental Medicine and Biology, 357–71. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4_16.
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Holzer, Peter, und Aitak Farzi. „Neuropeptides and the Microbiota-Gut-Brain Axis“. In Advances in Experimental Medicine and Biology, 195–219. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4_9.
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Soni, Awakash, Ankit Verma und Priya Gupta. „Microbiota–Gut–Brain Axis and Neurodegenerative Disorder“. In Nutritional Neurosciences, 27–46. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-4530-4_3.
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Sundaram, Soumya, Dinoop Korol Ponnambath und Sruthi S. Nair. „Microbiota-Gut-Brain Axis in Neurological Disorders“. In Human Microbiome, 147–67. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-7672-7_7.
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Naureen, Zakira, Saima Farooq, Tayyaba Zahoor und Syed Abdullah Gilani. „Effect of Probiotics on Gut Microbiota and Brain Interactions in the Context of Neurodegenerative and Neurodevelopmental Disorders“. In Microbiome-Gut-Brain Axis, 383–99. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-1626-6_19.
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Lyte, Mark. „Microbial Endocrinology and the Microbiota-Gut-Brain Axis“. In Advances in Experimental Medicine and Biology, 3–24. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4_1.
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Alonso, Carmen, María Vicario, Marc Pigrau, Beatriz Lobo und Javier Santos. „Intestinal Barrier Function and the Brain-Gut Axis“. In Advances in Experimental Medicine and Biology, 73–113. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4_4.
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Shin, Cheolmin, und Yong-Ku Kim. „Microbiota–Gut–Brain Axis: Pathophysiological Mechanism in Neuropsychiatric Disorders“. In Advances in Experimental Medicine and Biology, 17–37. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-7376-5_2.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Intestinal brain microbiota axis"
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Menezes, Carlos Alexandre Gomes Passarinho, Rafaela Ribeiro Benedito, Daniel Rubens Freitas Facundo, Isabela Oliveira Moura, Patrick Venâncio Soares Lima, Amandra Gabriele Coelho Rodrigues Melo, Bruna Gontijo Peixoto Pimenta et al. „Analysis of the intestinal microbiota and its relationship with neuropathologies“. In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.458.
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Introduction: The human intestinal microbiota corresponds to the ecosystem of colonizing microorganisms of the intestine that has an important role of protection to the organism. In addition, it has a direct relationship with the nervous system, known as the bowel-brain axis. Changes in the intestinal microbiota have been associated with several neuropathologies, and disbiosis repair has been shown to improve specific symptoms of some diseases. Objectives: This study aims to analyze the neurological implications caused by intestinal microbiota in humans. Methods: Review of integrative literature, consulted the Databases PubMed, SciELO and Google Academic. Chosen as descriptors (DeCS): “Microbiota”, “Gastrointestinal Microbiome” and “Nervous System Diseases” separated by Boolean connectors, and articles in English and Portuguese. Results: In this sense, among the therapeutic techniques that objectify to recolonize the “‘sick” intestine, the use of probiotics and fecal microbiota transplantation stand out. Symbiotics, a combination of probiotics and prebiotics, proved beneficial for symptomatological manifestations of neuropsychic disorders such as depression and chronic stress. Conclusion: Although some of the relationships of the intestinal-brain microbiota axis and changes in the intestinal microbiota, as well as the pathophysiology and benefits arising from its health, there is still a lack of studies to make consensus whether a change in the intestinal microbiome would be an epiphenomenon or the cause of neuropathologies in humans.
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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa und Edvaldo Cardoso. „Brain-gut-microbiota axis in motor disorders“. In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.401.
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Introduction: There seems to be a strong relationship and influence on the brain-gut- microbiota axis in the control and prevention of several diseases, including degenerative diseases that are related to motor disorders. Objectives: To analyze the relationship between movement disorders and the intestinal microbiota. Methods: Integrative review performed at PUBMED, using the descriptors Movement disorder and intestinal microbiota, in the last five years and having as inclusion criteria complete texts in English. Results: The literature suggests that the intestinal microbiota regulates the activation of microglia through the production of bacteria metabolites. Gut dysbiosis is believed to generate metabolic disorders with decreased production of neuroprotective factors, increased pro-inflammatory cytokines, production of neurotoxins, and a misdirected immune response. Metabolites produced by an altered microbiota seem to enter the circulation and affect neurological function. Braak’s hypothesis postulates that aberrant accumulation of α-synuclein (αSyn), a central component of the pathophysiology of Parkinson’s disease (PD), begins in the intestine and propagates through the vagus nerve to the brain, given that αSyn inclusions previously arise in the enteric nervous system and glossopharyngeal and vagus nerves, and vagotomized individuals have reduced risk of PD. Conclusion: The identification of the microbiota or its altered metabolites may serve as biomarkers, or even drug targets for the treatment of diseases of the central nervous system. The microbiota can be modulated through antibiotic therapy, fecal microbiota transplantation, prebiotic supplementation, dietary interventions and many other potential methods.
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Silva, Alexandre Almeida da, Lucas Cruz Furtado und Júlio César Claudino dos Santos. „Gut-microbiome-brain-axis: the crosstalk between the vagus nerve, alpha-synuclein and the brain in Parkinson’s disease“. In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.783.
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Introduction: The vagus nerve, the main component of the parasympathetic nervous system, is involved in the regulation of immune response, digestion, heart rate, and control of mood. It can detect microbiota metabolites through its afferents, transferring this gut information to the central nervous system. Preclinical and clinical studies have shown the important role played by the gut microbiome and gut-related factors in disease development and progression, as well as treatment responses. Objectives: To describe and discuss the close link between the microbiome, the gut and the brain in Parkinson’s disease. Methods: This is a critical review of the literature on the microbiome, gut, and brain in Parkinson’s disease. Results: The gut microbiota has been demonstrated to be a pivotal contributor to the promotion of health. Emerging data has indicated that, up to 20 years before the onset of motor symptoms, an alteration in the gut microbiome may be present in Parkinson’s disease patients. This dysbiosis of the gut may lead to increased intestinal permeability and inflammation, as well as Lewis body formation, and can also cause neuroinflammation and decreased neurotransmitter production in the central nervous system. Conclusion: More studies are needed to better understand the underlying biology and how this axis can be modulated for the patient’s benefit.
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Nogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira und Leiz Maria Costa Véras. „The autistic spectrum disorder and its relation to intestinal dysbiosis“. In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.283.
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Introduction: Autistic Spectrum Disorder (ASD) is characterized by a neurodevelopmental disorder, in which the child has persistent deficits in verbal and / or non-verbal communication, social interaction and behavior. One of the factors related to the cause of ASD are nutritional aspects, such as intestinal dysbiosis. Objective: To analyze the relationship between imbalance in the intestinal microbiota and the pathophysiological characteristics of ASD. Methodology: This is a systematic review, carried out in the Pubmed, SciELO databases, in order to answer the question: what is the relationship between intestinal microbiota imbalance and ASD? 139 articles were found, of which 12 were selected, through the simultaneous crossing between the descriptors “Autistic Disorder”, “Dysbiosis”. Articles written in Portuguese and English published from 2016 to 2021 were inserted. Results/Discussion: Most children with ASD exhibit gastrointestinal symptoms, such as constipation and diarrhea, and greater intestinal permeability, with major differences in the composition of microorganisms in the gastrointestinal tract (GIT). Patients with ASD have a lower microbiota diversity in the GIT. However, it is not possible to identify the origin of this change, since children with ASD often have changes in diet and eating behavior, which could alter the microbiota. Conclusion: It is still complex to understand what are the main causes of ASD. The gut-brain axis is an important associated factor both in the etiology and in the clinical manifestations of ASD. The use of diets, together with the modulation of the microbiota, by the use of probiotics and specific antibiotics, are possibilities for promising therapy.
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Li, Ting, Ning Ding, Hanqing Guo, Rui Hua, Zuyi Yuan und Yue Wu. „IDDF2022-ABS-0097 Aspirin impairs intestinal homeostasis through gut microbiota-bile-acids axis“. In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.2.
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Gopal, Pramod. „Human Gut Microbiota, Gut–Brain Axis and the Role of Diet“. In NSNZ 2021. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/msf2022009051.
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Lopes, Lorena Vieira, VINÍCIUS GRZECHOEZINSKI AUDINO und GABRIEL STECHECHEN WIER. „EIXO INTESTINO-PULMÃO E O PAPEL DA MICROBIOTA INTESTINAL NA RESPOSTA À INFECÇÃO POR SARS-COV-2“. In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6286.
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Introdução: A microbiota intestinal está relacionada à modulação do sistema imunológico, influenciando no processo inflamatório e na resposta a infecções. No curso da COVID-19, uma resposta exacerbada, na conhecida “tempestade de citocinas”, gera hiperinflamação e é fator determinante da gravidade da doença. Objetivo: Analisar os efeitos da microbiota intestinal na regulação da resposta imunológica à infecção por SARS-CoV-2 e seus mecanismos. Metodologia: Realizou-se revisão da literatura, a partir de publicações indexadas na plataforma PubMed. Foram utilizados os descritores “COVID-19”, “microbiome”, “inflammation” e “gut-lung axis”. Após avaliação criteriosa, foram selecionados 5 artigos para a presente revisão. Resultados: Foram relatadas associações entre a microbiota intestinal e a mortalidade por infecções respiratórias, sugerindo a existência de um eixo de comunicação bilateral “intestino-pulmão”. O possível mecanismo dessa interação é a atuação da microbiota na imunidade inata antiviral do trato respiratório através da liberação de metabólitos e sinais imunomodulatórios que influenciam macrófagos alveolares, células epiteliais e células dendríticas. O microbioma modula a expressão de receptores Interferon tipo I e secreção de IFN-α e IFN-β, com efeito na restrição da replicação viral. A alteração da composição da microbiota intestinal (disbiose) possivelmente guarda correlação positiva com a gravidade da COVID-19: observou-se aumento de táxons patogênicos e diminuição daqueles conhecidos por sua ação protetora, conforme maiores as taxas de complicações. A composição bacteriana intestinal em pacientes com doença leve se mostrou mais próxima a controles, enquanto casos graves e fatais apresentaram importante diferença em relação às bactérias protetoras. Maiores níveis de citocinas inflamatórias foram correlacionados à alteração da microbiota intestinal em pacientes hospitalizados com COVID-19. A disbiose intestinal prévia, comum em pacientes com comorbidades e idade avançada, também está ligada à desregulação da resposta inflamatória ao SARS-CoV-2. Conclusão: Os mecanismos que ligam a microbiota intestinal à resposta à infecção por SARS-CoV-2 não são totalmente compreendidos. Porém, os resultados sugerem correlação entre a composição da microbiota intestinal, reação inflamatória e o curso da COVID-19, constituindo uma rota promissora à compreensão da patogênese e elaboração de estratégias que diminuam o impacto da doença. Dessa forma, mais estudos são necessários para que essa relação seja estabelecida.
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Jin, Zeyongsheng, Yi Yin und Jing Zhu. „Effect of vitamin D on obesity and its role in the microbiota-gut-brain axis“. In International Conference on Biological Engineering and Medical Science (ICBIOMed2022), herausgegeben von Gary Royle und Steven M. Lipkin. SPIE, 2023. http://dx.doi.org/10.1117/12.2669654.
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Sergeyeva, Tatyana, Valeriy Sergeyev und Julia Kyznecova. „BACTERIOPHAGAL INFECTION OF RAT INTESTINAL MICROBIOTA INCREASES THE PERMEABILITY OF THE BLOOD-BRAIN BARRIER AND MIGRATION OF IMMUNE CELLS INTO THE BRAIN PARENCHYMA“. In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m548.sudak.ns2019-15/368-369.
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Maia, Lucas Henrique, Thaís Galdino Diniz, Vitor Carvalho Caetano, Marina Gomes Diniz, Pedro Lucas Bessa dos Reis, Gabriela Vieira Marques da Costa Leão, Vitor Moreira Nunes und Helton José dos Reis. „Antibiotic therapy as a risk factor in Parkinson’s disease“. In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.521.
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Background: Antibiotics exposure is related to gastrointestinal tract dysbiosis and appearance of systemic repercussions. Due to the correlation between Enteric Nervous System (ENS) and Central Nervous System (CNS), abnormalities in the gut microbiota have been associated with neurological disorders including Parkinson’s Disease (PD). Objectives: Search evidence in the scientific literature relating antibiotic therapy and Parkinson’s disease. Methods: A systematic review has been done using the descriptors “Parkinson’s disease”, “antibiotics” and “gut microbiota” in PubMed’s database. The research was conducted in april 2021, without temporal limitations, in english and portuguese. Results: Studies suggest that PD begins with intestinal inflammation and abnormal alpha-synuclein deposition in the ENS that follows, through nerves, to the CNS. Results show that leaky gut and dysbiosis preceded 5-10 years PD’s initial symptoms, while the intense exposure to antibiotics preceded 10-15 years the diagnostic. On average, PD patients received larger amounts of antibiotics than controls (p=0.021). Dysbiosis post-antibiotics presented reduced diversity of Bacteroidetes, Firmicutes and Prevotellaceae and growthing of Enterobacteriaceae, resulting in higher risk of gastrointestinal infections, higher rates of pro-inflammatory cytokines, increased permeability of gastrointestinal and brain-blood barriers and hyperexpression of the alpha-synuclein protein in the colon. Conclusion: Poorly controlled antibiotic therapy and its subsequent damage to gut microbiota anticipates PD’s early symptoms.