Related Experiment Video
Updated: Sep 1, 2025
Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice
Published on: September 19, 2019
The Microbiota-Gut-Brain Axis in Sepsis-Associated Encephalopathy
1Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California Davis, Davis, California, USA.
Abstract:
The gut microbiota is increasingly being found to contribute to the etiology and severity of multiple diseases, including within the central nervous system (CNS). This microbiota-gut-brain (MGB) axis facilitates communication between gut microbes and the brain to regulate behavior. Communication along the axis occurs via multiple routes, including the vagus nerve, gut-derived neurohormones, and immune cells, and more recently, a role for microbial metabolites has been uncovered. This commentary highlights the recent findings by H. Fang, Y. Wang, J. Deng, H. Zhang, et al. (mSystems 7:e01399-21, 2022, https://doi.org/10.1128/msystems.01399-21) on the role of gut microbiota and bacterial metabolites in mediating sepsis-associated encephalopathy in a mouse model of cecal puncture and ligation.
Insights
The gut microbiota influences brain health via the microbiota-gut-brain axis. Bacterial metabolites play a key role in sepsis-associated encephalopathy, impacting central nervous system function.
Area of Science:
- Microbiology
- Neuroscience
- Immunology
Background:
- The gut microbiota impacts numerous diseases, including central nervous system (CNS) disorders.
- The microbiota-gut-brain (MGB) axis describes bidirectional communication between gut microbes and the brain.
- Microbial metabolites are emerging as critical mediators in MGB axis signaling.
Purpose of the Study:
- To highlight recent findings on the role of gut microbiota and bacterial metabolites in sepsis-associated encephalopathy (SAE).
- To discuss the implications of these findings within the context of the MGB axis.
Main Methods:
- The study utilized a mouse model of cecal puncture and ligation to induce sepsis.
- Analysis focused on the role of gut microbiota and specific bacterial metabolites in SAE pathogenesis.
Main Results:
- Gut microbiota and their metabolites were found to mediate SAE in the studied mouse model.
- Specific bacterial metabolites contribute to the neurological complications associated with sepsis.
Conclusions:
- Gut microbiota and bacterial metabolites are significant contributors to SAE.
- Targeting the MGB axis and microbial metabolites may offer therapeutic strategies for sepsis-induced brain dysfunction.
