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Targeting the gut microbiome in the management of sepsis-associated encephalopathy

Brain injury resulting from sepsis, or sepsis-associated encephalopathy (SAE), occurs due to impaired end-organ perfusion, dysregulated inflammation affecting the central nervous system (CNS), blood-brain barrier (BBB) disruption, mitochondrial dysfunction, oxidative stress, accumulation of toxic ne...

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Detalles Bibliográficos
Autores principales: Barlow, Brooke, Ponnaluri, Sameer, Barlow, Ashley, Roth, William
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9557965/
https://www.ncbi.nlm.nih.gov/pubmed/36247756
http://dx.doi.org/10.3389/fneur.2022.999035
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author Barlow, Brooke
Ponnaluri, Sameer
Barlow, Ashley
Roth, William
author_facet Barlow, Brooke
Ponnaluri, Sameer
Barlow, Ashley
Roth, William
author_sort Barlow, Brooke
collection PubMed
description Brain injury resulting from sepsis, or sepsis-associated encephalopathy (SAE), occurs due to impaired end-organ perfusion, dysregulated inflammation affecting the central nervous system (CNS), blood-brain barrier (BBB) disruption, mitochondrial dysfunction, oxidative stress, accumulation of toxic neuropeptides and impaired toxin clearance secondary to sepsis-induced hepatic and renal dysfunction. The gut microbiome becomes pathologically altered in sepsis, which likely contributes to the pathogenesis of SAE. Herein, we review the literature detailing dysregulation of microbiota-gut-brain axis (MGBA) in SAE and highlight potential therapeutic strategies to modulate the gut microbiome to mitigate sepsis-induced brain injury.
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spelling pubmed-95579652022-10-14 Targeting the gut microbiome in the management of sepsis-associated encephalopathy Barlow, Brooke Ponnaluri, Sameer Barlow, Ashley Roth, William Front Neurol Neurology Brain injury resulting from sepsis, or sepsis-associated encephalopathy (SAE), occurs due to impaired end-organ perfusion, dysregulated inflammation affecting the central nervous system (CNS), blood-brain barrier (BBB) disruption, mitochondrial dysfunction, oxidative stress, accumulation of toxic neuropeptides and impaired toxin clearance secondary to sepsis-induced hepatic and renal dysfunction. The gut microbiome becomes pathologically altered in sepsis, which likely contributes to the pathogenesis of SAE. Herein, we review the literature detailing dysregulation of microbiota-gut-brain axis (MGBA) in SAE and highlight potential therapeutic strategies to modulate the gut microbiome to mitigate sepsis-induced brain injury. Frontiers Media S.A. 2022-09-29 /pmc/articles/PMC9557965/ /pubmed/36247756 http://dx.doi.org/10.3389/fneur.2022.999035 Text en Copyright © 2022 Barlow, Ponnaluri, Barlow and Roth. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neurology
Barlow, Brooke
Ponnaluri, Sameer
Barlow, Ashley
Roth, William
Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title_full Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title_fullStr Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title_full_unstemmed Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title_short Targeting the gut microbiome in the management of sepsis-associated encephalopathy
title_sort targeting the gut microbiome in the management of sepsis-associated encephalopathy
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9557965/
https://www.ncbi.nlm.nih.gov/pubmed/36247756
http://dx.doi.org/10.3389/fneur.2022.999035
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