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Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.
El Baassiri, Mahmoud G; Raouf, Zachariah; Badin, Sarah; Escobosa, Alejandro; Sodhi, Chhinder P; Nasr, Isam W.
Afiliação
  • El Baassiri MG; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
  • Raouf Z; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
  • Badin S; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
  • Escobosa A; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
  • Sodhi CP; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
  • Nasr IW; Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA. inasr1@jhmi.edu.
J Neuroinflammation ; 21(1): 124, 2024 May 10.
Article em En | MEDLINE | ID: mdl-38730498
ABSTRACT
Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack of effective treatments underscore the urgent need for innovative therapeutic strategies. The brain-gut axis has emerged as a crucial bidirectional pathway connecting the brain and the gastrointestinal (GI) system through an intricate network of neuronal, hormonal, and immunological pathways. Four main pathways are primarily implicated in this crosstalk, including the systemic immune system, autonomic and enteric nervous systems, neuroendocrine system, and microbiome. TBI induces profound changes in the gut, initiating an unrestrained vicious cycle that exacerbates brain injury through the brain-gut axis. Alterations in the gut include mucosal damage associated with the malabsorption of nutrients/electrolytes, disintegration of the intestinal barrier, increased infiltration of systemic immune cells, dysmotility, dysbiosis, enteroendocrine cell (EEC) dysfunction and disruption in the enteric nervous system (ENS) and autonomic nervous system (ANS). Collectively, these changes further contribute to brain neuroinflammation and neurodegeneration via the gut-brain axis. In this review article, we elucidate the roles of various anti-inflammatory pharmacotherapies capable of attenuating the dysregulated inflammatory response along the brain-gut axis in TBI. These agents include hormones such as serotonin, ghrelin, and progesterone, ANS regulators such as beta-blockers, lipid-lowering drugs like statins, and intestinal flora modulators such as probiotics and antibiotics. They attenuate neuroinflammation by targeting distinct inflammatory pathways in both the brain and the gut post-TBI. These therapeutic agents exhibit promising potential in mitigating inflammation along the brain-gut axis and enhancing neurocognitive outcomes for TBI patients.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Lesões Encefálicas Traumáticas / Eixo Encéfalo-Intestino / Anti-Inflamatórios Limite: Animals / Humans Idioma: En Revista: J Neuroinflammation Assunto da revista: NEUROLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Lesões Encefálicas Traumáticas / Eixo Encéfalo-Intestino / Anti-Inflamatórios Limite: Animals / Humans Idioma: En Revista: J Neuroinflammation Assunto da revista: NEUROLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos
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