Abstract
Traumatic brain injury (TBI) has profound effects that extend beyond the brain, affecting
other body systems via secondary pathways and leading to various complications, including
gastrointestinal (GI) dysfunction during and after hospitalization. While advances
in TBI management have improved overall outcomes, the absence of effective treatments
for these systemic effects highlights the urgent need for innovative therapeutic strategies.
A critical aspect in this context is the brain–gut axis (BGA), a bidirectional communication
network connecting the brain and GI system through complex neuronal, hormonal, and
immune pathways. TBI results in increased intestinal permeability and a hypercatabolic
state leading to bacterial translocation, immune dysregulation, septic complications,
and multiorgan failure. These complications significantly heighten the risk of morbidity
and mortality in TBI patients. Emerging evidence suggests that gut dysbiosis plays
a pivotal role in post-TBI complications. The gut microbiome, a diverse community
of commensal microorganisms, is integral to gut physiology, performing key functions
such as metabolic regulation, maintaining the intestinal barrier, and modulating immune
responses. Disruptions to this microbiota can exacerbate GI and immune system dysfunction,
potentially leading to severe outcomes. This review examines the mechanisms underlying
BGA dysfunction following TBI, focusing on the pathways contributing to this dysregulation.
Additionally, it discusses therapeutic strategies aimed at mitigating gut microbiota
dysbiosis. Potential interventions include approaches to restore microbial balance,
enhance gut barrier integrity, and support immune modulation. By targeting these areas,
therapies may reduce the systemic effects of TBI and improve patient outcomes.
Keywords
traumatic brain injury - brain–gut axis - microbiome - dysbiosis - therapeutic interventions
