Preventive effects of GABA-producing postbiotics derived from Levilactobacillus brevis against chronic sleep deprivation-induced gut-brain axis dysfunction, neuroinflammation, and behavioral impairments in mice

Feb 7, 2026Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

GABA-producing postbiotics from Levilactobacillus brevis may protect against gut-brain problems, brain inflammation, and behavior issues caused by long-term sleep loss in mice

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Abstract

GABA-producing postbiotics significantly alleviated anxiety- and depression-like behaviors in mice subjected to 30 days of chronic sleep deprivation.

Chronic sleep deprivation is associated with gut dysbiosis and increased systemic inflammation.
Treatment with GABA-producing postbiotics restored intestinal tight junction protein expression and improved intestinal barrier function.
Postbiotic treatment increased antioxidant activity and reduced markers of systemic inflammation, such as serum lipopolysaccharide and TNF-α levels.
Beneficial gut bacteria, including Ruminococcus and Akkermansia, were promoted by postbiotic treatment, along with increased fecal propanoic acid concentrations.
In the brain, postbiotics upregulated genes related to the blood-brain barrier and reduced expressions of neuroinflammatory genes.
Microbial signatures correlated with levels of short-chain fatty acids and other markers of inflammation and gut integrity.

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Chronic sleep deprivation (CSD) is increasingly recognized as a contributor to gut dysbiosis, systemic inflammation, and neurobehavioral impairments via the gut-brain axis. γ-Aminobutyric acid (GABA)-producing postbiotics, derived from microbial fermentation, offer potential in mitigating such dysfunctions. This study investigates the effects of GABA-producing postbiotics produced by Levilactobacillus brevis on CSD-induced gut and brain disturbances in mice. Male C57BL/6 mice were subjected to 30 days of sleep fragmentation and treated with low (250 mg/kg) or high (500 mg/kg) doses of postbiotics. Behavioral tests revealed that GABA-producing postbiotics significantly alleviated anxiety- and depression-like behaviors. Postbiotic treatment restored intestinal tight junction protein expression (ZO-1, Claudin-1), increased glutathione peroxidase activity, and reduced serum lipopolysaccharide and TNF-α levels, indicating improved intestinal barrier function and attenuated systemic inflammation. Postbiotic treatment promote the growth of beneficial genera such as Ruminococcus and Akkermansia, while also elevating fecal propanoic acid concentrations. In the brain, postbiotics upregulated blood-brain barrier (BBB) associated genes and reduced neuroinflammatory gene expression. Correlation analysis highlighted microbial signatures linked to short-chain fatty acids, intestinal tight junction proteins, serum LPS and TNF-α levels, as well as hypothalamic inflammatory, BBB gene expressions and anxiety. These findings suggest that GABA-producing postbiotics ameliorate CSD-induced gut-brain axis disruption by modulating the microbiota, restoring barrier functions, and suppressing systemic and neuroinflammation. This study supports the potential application of GABA-producing postbiotics as a dietary strategy to mitigate sleep loss-related physiological and behavioral impairments.

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Preventive effects of GABA-producing postbiotics derived from Levilactobacillus brevis against chronic sleep deprivation-induced gut-brain axis dysfunction, neuroinflammation, and behavioral impairments in mice

Abstract

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