Citation

Celorrio M, Friess SH. Neural Regen. Res. 2022; 17(5): 1007-1008.

Copyright

(Copyright © 2022, Neural Regeneration Research, Shenyang, Liaoning Province, P.R. China, Publisher Wolters Kluwer)

DOI

10.4103/1673-5374.324839

PMID

unavailable

Abstract

The gastrointestinal track is inhabited by tens of trillions of microorganisms. The gut microbiota is involved in gut motility, nutrient absorption and synthesis of metabolites that influence homeostasis, metabolism and immune function. Given the influence gut microbiota has on health, there is a growing body of literature describing the gut microbiota’s impact on brain and behavior. The bidirectional nature of the gut-brain axis involves neurological, immunological and hormonal mechanisms that can induce perturbations in gut or brain homeostasis. Studies using different but complementary approaches, such as germ free mice, antibiotics, probiotics, gastrointestinal infection, and fecal microbiota transplant, have shown that the gut microbiota acting via the gut-brain axis contribute to the regulation of brain and behavior, impacting depression, stress and cognition. Moreover, gut microbiota disruption has been associated with neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and implicated in modulating disease severity in stroke. Traumatic brain injury (TBI) is a complex, acute neurological insult that can lead to chronic neurodegeneration. Understanding the influence of the gut-brain axis in the setting of TBI may create new avenues of therapeutic approaches for TBI survivors.

Preclinical investigations provide evidence that TBI can impact intestinal function and the gut microbiota. In a moderate TBI rat model utilizing 16S rRNA sequencing of stool, changes in gut microbiota were detected as early as 2 days after injury (Nicholson et al., 2019). TBI’s impact on gut microbiota may be long-lasting with significant changes in gut bacterial populations for up to 28 days after injury (Opeyemi et al., 2021). Larger lesion volume was associated with alterations of gut microbiota that may influence functional outcome. In another preclinical study of diffuse brain injury, TBI-induced microbial dysbiosis with gastrointestinal dysfunction and alteration of bile acid was an important mediator of gut microbiome-host interactions (You et al., 2021). Gut microbial dysbiosis was associated with decreased levels of bile acid in feces and plasma. This study supported the hypothesis that TBI-induced gut microbial dysbiosis contributed to intestinal inflammation by decreasing bile acid (You et al., 2021). Fecal microbiota transplant for 7 days after TBI in rats restored gut microbiota, improving neurological outcomes and exerting an anti-oxidative effect via decreasing TBI-induced trimethylamine N-oxide, a gut microbiota metabolite, and increasing the antioxidant enzyme methionine sulfoxide reductase A expression in the hippocampus (Du et al., 2021). This data supports the concept that the gut-brain axis is bidirectional and TBI can induce alterations in the gut microbiome.

The composition of the gut microbiota is shaped significantly by the immune system and resident microbes provide signals for normal immune system development. Disruption of the gut-immune axis induces profound consequences in host health. However, there are still major gaps in our understanding of how the immune system can regulate microbiota and how ...

Language: en