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dc.contributor.authorSundman, Mark H.
dc.contributor.authorChen, Nan-kuei
dc.contributor.authorSubbian, Vignesh
dc.contributor.authorChou, Ying-hui
dc.date.accessioned2017-11-22T23:44:04Z
dc.date.available2017-11-22T23:44:04Z
dc.date.issued2017-11
dc.identifier.citationThe bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease 2017, 66:31 Brain, Behavior, and Immunityen
dc.identifier.issn08891591
dc.identifier.doi10.1016/j.bbi.2017.05.009
dc.identifier.urihttp://hdl.handle.net/10150/626124
dc.description.abstractAs 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.
dc.language.isoenen
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCEen
dc.relation.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0889159117301551en
dc.rights© 2017 Elsevier Inc. All rights reserved.en
dc.subjectGut-brain axisen
dc.subjectTraumatic Brain Injuryen
dc.subjectConcussionen
dc.subjectGuten
dc.subjectMicrobiotaen
dc.subjectChronic Traumatic Encephalopathyen
dc.subjectNeurodegenerative diseaseen
dc.subjectNeuroinflammationen
dc.subjectMicrogliaen
dc.subjectIntestinal dysfunctionen
dc.titleThe bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and diseaseen
dc.typeArticleen
dc.contributor.departmentDepartment of Psychology, University of Arizona, Tucson, AZ, USAen
dc.identifier.journalBrain, Behavior, and Immunityen
dc.description.note12 month embargo; Available online 17 May 2017.en
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en
dc.eprint.versionFinal accepted manuscripten
refterms.dateFOA2018-05-18T00:00:00Z
html.description.abstractAs 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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