Gut microbiota dysbiosis shapes brain T-cell immunity in accelerated aging.
Abstract
The bidirectional communication between the gut microbiota, immune system, and central nervous system-the gut‒brain axis-plays a vital role in maintaining brain health. Its disruption can lead to neuroinflammation and cognitive decline. However, the relationship between the gut microbiota and age-related changes in brain immunity remains unclear. This study examined gut microbiota composition and T-cell profiles in senescence-accelerated SAMP8 mice and senescence-resistant SAMR1 controls at young adult and aged stages. The accelerated-aging phenotype of SAMP8 mice was confirmed by reduced behavioral performance and brain transcriptomic alterations. Fecal microbiota profiles were obtained using culture-dependent plating and 16S rRNA gene sequencing. T-cell phenotypes were determined by flow cytometry on brain and splenic leukocytes. Strain, age, and sex were drivers of microbiota composition variation. Microbial diversity differed between strains independently of age. Several bacterial genera had altered abundances in young SAMP8 mice, with only
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Research summary
The study demonstrates that gut microbiota dysbiosis in senescence-accelerated SAMP8 mice drives specific alterations in brain T-cell immunity, linking microbial composition to neuroinflammation in an accelerated aging model. This is relevant because it investigates the mechanistic pathways of the gut-brain axis that contribute to age-related immune decline and neurodegeneration, offering potential targets for interventions aimed at preserving brain health during aging, though the use of a specific mouse strain limits the generalizability of the findings to human longevity.
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