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Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)

Understanding the relationship between microorganisms that live in our intestines and neuroinflammatory and neurodegenerative pathologies of the central nervous system (CNS) is essential, since they have been shown to have an immunomodulatory effect in neurological disorders, such as multiple sclero...

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Autores principales: Torres-Chávez, María Eugenia, Torres-Carrillo, Nora Magdalena, Monreal-Lugo, Ana Victoria, Garnés-Rancurello, Sandra, Murugesan, Selvasankar, Gutiérrez-Hurtado, Itzae Adonai, Beltrán-Ramírez, Jesús Raúl, Sandoval-Pinto, Elena, Torres-Carrillo, Norma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10603378/
https://www.ncbi.nlm.nih.gov/pubmed/37901876
http://dx.doi.org/10.3892/br.2023.1675
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author Torres-Chávez, María Eugenia
Torres-Carrillo, Nora Magdalena
Monreal-Lugo, Ana Victoria
Garnés-Rancurello, Sandra
Murugesan, Selvasankar
Gutiérrez-Hurtado, Itzae Adonai
Beltrán-Ramírez, Jesús Raúl
Sandoval-Pinto, Elena
Torres-Carrillo, Norma
author_facet Torres-Chávez, María Eugenia
Torres-Carrillo, Nora Magdalena
Monreal-Lugo, Ana Victoria
Garnés-Rancurello, Sandra
Murugesan, Selvasankar
Gutiérrez-Hurtado, Itzae Adonai
Beltrán-Ramírez, Jesús Raúl
Sandoval-Pinto, Elena
Torres-Carrillo, Norma
author_sort Torres-Chávez, María Eugenia
collection PubMed
description Understanding the relationship between microorganisms that live in our intestines and neuroinflammatory and neurodegenerative pathologies of the central nervous system (CNS) is essential, since they have been shown to have an immunomodulatory effect in neurological disorders, such as multiple sclerosis (MS). The gut microbiota can be affected by several environmental factors, including infections, physical and emotional stress and diet, the latter known as the main modulator of intestinal bacteria. An abrupt shift in the gut microbiota composition and function is known as dysbiosis, a state of local and systemic inflammation produced by pathogenic bacteria and its metabolites responsible for numerous neurological symptoms. It may also trigger neuronal damage in patients diagnosed with MS. Intestinal dysbiosis affects the permeability of the intestine, allowing chronic low-grade bacterial translocation from the intestine to the circulation, which may overstimulate immune cells and cells resident in the CNS, break immune tolerance and, in addition, alter the permeability of the blood-brain barrier (BBB). This way, toxins, inflammatory molecules and oxidative stress molecules can pass freely into the CNS and cause extensive damage to the brain. However, commensal bacteria, such as the Lactobacillus genus and Bacteroides fragilis, and their metabolites (with anti-inflammatory potential), produce neurotransmitters such as γ-aminobutyric acid, histamine, dopamine, norepinephrine, acetylcholine and serotonin, which are important for neurological regulation. In addition, reprogramming the gut microbiota of patients with MS with a healthy gut microbiota may help improve the integrity of the gut and BBB, by providing clinically protective anti-inflammatory effects and reducing the disease's degenerative progression. The present review provides valuable information about the relationship between gut microbiota and neuroinflammatory processes of the CNS. Most importantly, it highlights the importance of intestinal bacteria as an environmental factor that may mediate the clinical course of MS, or even predispose to the outbreak of this disease.
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spelling pubmed-106033782023-10-28 Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review) Torres-Chávez, María Eugenia Torres-Carrillo, Nora Magdalena Monreal-Lugo, Ana Victoria Garnés-Rancurello, Sandra Murugesan, Selvasankar Gutiérrez-Hurtado, Itzae Adonai Beltrán-Ramírez, Jesús Raúl Sandoval-Pinto, Elena Torres-Carrillo, Norma Biomed Rep Review Understanding the relationship between microorganisms that live in our intestines and neuroinflammatory and neurodegenerative pathologies of the central nervous system (CNS) is essential, since they have been shown to have an immunomodulatory effect in neurological disorders, such as multiple sclerosis (MS). The gut microbiota can be affected by several environmental factors, including infections, physical and emotional stress and diet, the latter known as the main modulator of intestinal bacteria. An abrupt shift in the gut microbiota composition and function is known as dysbiosis, a state of local and systemic inflammation produced by pathogenic bacteria and its metabolites responsible for numerous neurological symptoms. It may also trigger neuronal damage in patients diagnosed with MS. Intestinal dysbiosis affects the permeability of the intestine, allowing chronic low-grade bacterial translocation from the intestine to the circulation, which may overstimulate immune cells and cells resident in the CNS, break immune tolerance and, in addition, alter the permeability of the blood-brain barrier (BBB). This way, toxins, inflammatory molecules and oxidative stress molecules can pass freely into the CNS and cause extensive damage to the brain. However, commensal bacteria, such as the Lactobacillus genus and Bacteroides fragilis, and their metabolites (with anti-inflammatory potential), produce neurotransmitters such as γ-aminobutyric acid, histamine, dopamine, norepinephrine, acetylcholine and serotonin, which are important for neurological regulation. In addition, reprogramming the gut microbiota of patients with MS with a healthy gut microbiota may help improve the integrity of the gut and BBB, by providing clinically protective anti-inflammatory effects and reducing the disease's degenerative progression. The present review provides valuable information about the relationship between gut microbiota and neuroinflammatory processes of the CNS. Most importantly, it highlights the importance of intestinal bacteria as an environmental factor that may mediate the clinical course of MS, or even predispose to the outbreak of this disease. D.A. Spandidos 2023-10-12 /pmc/articles/PMC10603378/ /pubmed/37901876 http://dx.doi.org/10.3892/br.2023.1675 Text en Copyright: © Torres-Chávez et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Review
Torres-Chávez, María Eugenia
Torres-Carrillo, Nora Magdalena
Monreal-Lugo, Ana Victoria
Garnés-Rancurello, Sandra
Murugesan, Selvasankar
Gutiérrez-Hurtado, Itzae Adonai
Beltrán-Ramírez, Jesús Raúl
Sandoval-Pinto, Elena
Torres-Carrillo, Norma
Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title_full Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title_fullStr Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title_full_unstemmed Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title_short Association of intestinal dysbiosis with susceptibility to multiple sclerosis: Evidence from different population studies (Review)
title_sort association of intestinal dysbiosis with susceptibility to multiple sclerosis: evidence from different population studies (review)
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10603378/
https://www.ncbi.nlm.nih.gov/pubmed/37901876
http://dx.doi.org/10.3892/br.2023.1675
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