Gut microbiota modulates the inflammatory response and cognitive impairment induced by sleep deprivation
Abstract
Sleep deprivation (SD) is increasingly common in modern society, which can lead to the dysregulation of inflammatory responses and cognitive impairment, but the mechanisms remain unclear. Emerging evidence suggests that gut microbiota plays a critical role in the pathogenesis and development of inflammatory and psychiatric diseases, possibly via gut microbiota-brain interactions and neuroinflammation. The present study investigated the impact of SD on gut microbiota composition and explored whether alterations of the gut microbiota play a causal role in chronic inflammatory states and cognitive impairment that are induced by SD. We found that SD-induced gut dysbiosis, inflammatory responses, and cognitive impairment in humans. Moreover, the absence of the gut microbiota suppressed inflammatory response and cognitive impairment induced by SD in germ-free (GF) mice. Transplantation of the "SD microbiota" into GF mice activated the Toll-like receptor 4/nuclear factor-κB signaling pathway and impaired cognitive function in the recipient mice. Mice that harbored "SD microbiota" also exhibited increases in neuroinflammation and microglial activity in the hippocampus and medial prefrontal cortex. These findings indicate that gut dysbiosis contributes to both peripheral and central inflammatory processes and cognitive deficits that are induced by SD, which may open avenues for potential interventions that can relieve the detrimental consequences of sleep loss.
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Sleep deprivation induces gut dysbiosis and intestinal barrier disruption, leading to microglial activation and cognitive decline.
“sleep deprivation (SD) induces gut dysbiosis and intestinal barrier disruption, leading to microglial activation and cognitive decline”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [647]
Sleep deprivation in humans induced depletion of SCFAs-producing species and systemic inflammation via activation of the TLR4/NF-κB signaling pathway.
“SD in humans induced depletion of SCFAs-producing species, systemic inflammation via the activation of TLR4/NF-κB signaling pathway.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [647]
GF sleep-deprived mice exhibited weaker inflammatory responses, reduced intestinal barrier damage, and milder cognitive impairment as compared to their SPF counterparts, highlighting the crucial role of gut microbiota in mediating sleep deprivation-induced pathological changes.
“GF sleep-deprived mice exhibited weaker inflammatory responses, reduced intestinal barrier damage, and milder cognitive impairment as compared to their SPF counterparts, highlighting the crucial role of gut microbiota in mediating SD-induced pathological changes.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [647]
FMT from sleep-deprived humans to GF mice significantly reduced SCFAs levels, promoted both peripheral and central inflammatory responses, and impaired cognitive function.
“FMT from SD human to GF mice significantly reduced SCFAs levels, promoted both peripheral and central inflammatory responses, and impaired cognitive function.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [647]
This is coupled with increased serum levels of zonulin and S100β, indicating compromised intestinal barrier and BBB.
“This is coupled with increased serum levels of zonulin and S100β, indicating compromised intestinal barrier and BBB.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [647]
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References 87 · Cited by 307
- Authors
- Wang, Z., Chen, W.-H., Li, S.-X., He, Z.-M., Zhu, W.-L., Ji, Y.-B., Wang, Z., Zhu, X.-M., Yuan, K., Bao, Y.-P., Shi, L., Meng, S.-Q., Xue, Y.-X., Xie, W., Shi, J., Yan, W., Wei, H., Lu, L., & Han, Y.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Peking University (CN)
- Army Medical University (CN)
- Anhui Mental Health Center (CN)
- Sun Yat-sen University (CN)
- Corresponding author
- Yan, Wei
- Wei, Hong
- Han, Ying
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2021-05-07
- Volume
- 26
- Issue
- 11
- Pages
- 6277-6292
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W3158878919
- Cited by
- 307
- References
- 87
- Citations by year
- 2026: 60 · 2025: 76 · 2024: 87 · 2023: 50 · 2022: 34
- FWCI
- 13.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Key Research and Development Program of China
- National Natural Science Foundation of China (81901347, 31800897, 81770434, 81821092)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Keywords
- sleep deprivation, gut microbiota, gut dysbiosis, neuroinflammation, cognitive impairment, germ-free mice, microbiota transplantation, TLR4, NF-κB signaling, microglial activation, hippocampus, medial prefrontal cortex, gut-brain axis, chronic inflammation
- MeSH terms
- Gastrointestinal Microbiome, Animals, Inflammation, Sleep Deprivation, Mice, Cognitive Dysfunction, Dysbiosis
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