Michela Ferrara 1 , Giuseppe Bertozzi 2 , Christian Zanza 3 , Yaroslava Longhitano 4 , Fabio Piccolella 4 , Cristiano Ernesto Lauritano 4 , Gianpietro Volonnino 1 , Alice Chiara Manetti 5 , Aniello Maiese 5 , Raffaele La Russa 6 . Show Affiliations »
Abstract
BACKGROUND: Traumatic brain injury (TBI) can be considered as a "silent epidemic", causing morbidity, disability, and mortality in all-age cohorts. Therefore, a greater understanding of the underlying pathophysiological intricate mechanisms and interactions with other organs and systems is necessary to intervene not only in the treatment but also in the prevention of complications. In this complex of reciprocal influences, the complex brain-gut axis has captured a growing interest. SCOPE: The purpose of this manuscript is to examine and systematize existing evidence regarding the pathophysiological processes that occur following TBI and the influences exerted on these by the brain-gut axis. LITERATURE REVIEW: A systematic review of the literature was conducted according to the PRISMA methodology. On the 8th of October 2021, two independent databases were searched: PubMed and Scopus. Following the inclusion and exclusion criteria selected, 24 (12 from PubMed and 12 from Scopus) eligible manuscripts were included in the present review. Moreover, references of the selected articles were also revised following the criteria mentioned above, reaching 91 included manuscripts. DISCUSSION: Published evidence suggests that the brain and gut mutually influence through four main pathways: microbiota, inflammatory, nervous, endocrine. CONCLUSION: These pathways are bidirectional and influence each other. However, the studies conducted so far mainly involve animals. An autopsy methodological approach to corpses affected by traumatic brain injury or intestinal pathology could represent the keystone for future studies to clarify the complex pathophysiological processes underlying the interaction between these two main systems. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
BACKGROUND: Traumatic brain injury (TBI) can be considered as a "silent epidemic", causing morbidity, disability, and mortality in all-age cohorts. Therefore, a greater understanding of the underlying pathophysiological intricate mechanisms and interactions with other organs and systems is necessary to intervene not only in the treatment but also in the prevention of complications. In this complex of reciprocal influences, the complex brain-gut axis has captured a growing interest. SCOPE: The purpose of this manuscript is to examine and systematize existing evidence regarding the pathophysiological processes that occur following TBI and the influences exerted on these by the brain-gut axis. LITERATURE REVIEW: A systematic review of the literature was conducted according to the PRISMA methodology. On the 8th of October 2021, two independent databases were searched: PubMed and Scopus. Following the inclusion and exclusion criteria selected, 24 (12 from PubMed and 12 from Scopus) eligible manuscripts were included in the present review. Moreover, references of the selected articles were also revised following the criteria mentioned above, reaching 91 included manuscripts. DISCUSSION: Published evidence suggests that the brain and gut mutually influence through four main pathways: microbiota, inflammatory, nervous, endocrine. CONCLUSION: These pathways are bidirectional and influence each other. However, the studies conducted so far mainly involve animals. An autopsy methodological approach to corpses affected by traumatic brain injury or intestinal pathology could represent the keystone for future studies to clarify the complex pathophysiological processes underlying the interaction between these two main systems. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities: Chemical
Keywords:
dysautonomia; dysbiosis; gut-brain axis; microbiota.; neuroinflammation; traumatic brain injury
Year: 2022
PMID: 35733301 DOI: 10.2174/1574887117666220622143423
Source DB: PubMed Journal: Rev Recent Clin Trials ISSN: 1574-8871