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A brief period of sleep deprivation leads to subtle changes in mouse gut microbiota.

ABSTRACT: Not getting enough sleep is a common problem in our society and contributes to numerous health problems, including high blood pressure, diabetes and obesity. Related to these observations, a wealth of studies has underscored the negative impact of both acute and chronic sleep deprivation on cognitive function. More recently it has become apparent that the gut microbiota composition can be rapidly altered, modulates brain function and is affected by the aforementioned health problems. As such, changes in the microbiota composition may contribute to the behavioural and physiological phenotypes associated with sleep deprivation. It is unclear, however, whether a brief period of sleep deprivation can also negatively impact the gut microbiota. Here, we examined the impact of 5 hr of sleep deprivation on gut microbiota composition of male C57Bl6/J mice. Despite the fact that the overall microbial composition did not change between the control- and sleep-deprived groups, the relative abundance of the Clostridiaceae and Lachnospiraceae were slightly altered in sleep-deprived animals compared to controls. Together, these data suggest that depriving mice of sleep for 5 hr leads to subtle changes in the gut microbiota composition.

SUBMITTER: El Aidy S

PROVIDER: S-EPMC7757181 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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A brief period of sleep deprivation leads to subtle changes in mouse gut microbiota.

El Aidy Sahar S Bolsius Youri G YG Raven Frank F Havekes Robbert R

Journal of sleep research 20190912 6

Not getting enough sleep is a common problem in our society and contributes to numerous health problems, including high blood pressure, diabetes and obesity. Related to these observations, a wealth of studies has underscored the negative impact of both acute and chronic sleep deprivation on cognitive function. More recently it has become apparent that the gut microbiota composition can be rapidly altered, modulates brain function and is affected by the aforementioned health problems. As such, ch ...[more]

PMID: 31515894

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Project description:ObjectiveSleep deprivation has developed into a common phenomenon, which can lead to inflammatory responses and cognitive impairment, but the underlying mechanism is ambiguous. Emerging evidence shows that gut microbiota plays a crucial role in theoccurrence and development of inflammatory and psychiatric diseases, possibly through neuroinflammation and the brain-gut axis. The current study investigated the influence of sleep deprivation on gut microbiota composition, pro-inflammatory cytokines, learning and memory in mice. Further, it explored whether changes in gut microbiota increase pro-inflammatory cytokine and induce learning and memory impairment.MethodsHealthy 8-week-old male C57BL/6J mice were randomly divided into the regular control group (RC), environmental control group (EC), and sleep deprivation group (SD). The sleep deprivation model was established by the Modified Multiple Platform Method. The experimental mice were subjected to sleep deprivation for 6h/d (8:00 am∼14:00 pm) in a sleep deprivation chamber, and the duration of sleep deprivation was 8 weeks. Morris water maze test to assess learning and memory in mice. Enzyme-Linked Immunosorbent Assay determined the concentrations of inflammatory cytokines. The changes in gut microbiota in mice were analyzed by 16S rRNA sequencing.ResultsWe found that SD mice had elevated latency of exploration to reach the hidden platform (p>0.05) and significantly decreased traversing times, swimming distance, and swimming time in the target zone when the hidden platform was removed (p<0.05). Sleep deprivation caused dysregulated expression in serum IL-1β, IL-6, and TNF-α in mice, and the difference was significant (all p<0.001). Tannerellaceae, Rhodospirillales, Alistipes, and Parabacteroides were significantly increased in SD mice. Correlation analysis showed IL-1β was positively correlated with the abundance of Muribaculaceae (r=0.497, p<0.05) and negatively correlated with the abundance of Lachnospiraceae (r=-0.583, p<0.05). The TNF-α was positively correlated with the abundances of Erysipelotrichaceae, Burkholderiaceae, and Tannerellaceae (r=0.492, r=0.646, r=0.726, all p<0.05).ConclusionSleep deprivation can increase pro-inflammatory cytokine responses and learning and memory impairment in mice and may be caused by the disorder of the microbiota. These findings of this study may open avenues for potential interventions that can relieve the detrimental consequences of sleep loss.

Project description:Background Sleep loss is a serious global health concern. Consequences include memory deficits and gastrointestinal dysfunction. Our previous research showed that melatonin can effectively improve cognitive impairment and intestinal microbiota disturbances caused by sleep deprivation (SD). The present study further explored the mechanism by which exogenous melatonin prevents SD-induced cognitive impairments. Here, we established fecal microbiota transplantation, Aeromonas colonization and LPS or butyrate supplementation tests to evaluate the role of the intestinal microbiota and its metabolites in melatonin in alleviating SD-induced memory impairment. Results Transplantation of the SD-gut microbiota into normal mice induced microglia overactivation and neuronal apoptosis in the hippocampus, cognitive decline, and colonic microbiota disorder, manifesting as increased levels of Aeromonas and LPS and decreased levels of Lachnospiraceae_NK4A136 and butyrate. All these events were reversed with the transplantation of SD + melatonin-gut microbiota. Colonization with Aeromonas and the addition of LPS produced an inflammatory response in the hippocampus and spatial memory impairment in mice. These changes were reversed by supplementation with melatonin, accompanied by decreased levels of Aeromonas and LPS. Butyrate administration to sleep-deprived mice restored inflammatory responses and memory impairment. In vitro, LPS supplementation caused an inflammatory response in BV2 cells, which was improved by butyrate supplementation. This ameliorative effect of butyrate was blocked by pretreatment with MCT1 inhibitor and HDAC3 agonist but was mimicked by TLR4 and p-P65 antagonists. Conclusions Gut microbes and their metabolites mediate the ameliorative effects of melatonin on SD-induced cognitive impairment. A feasible mechanism is that melatonin downregulates the levels of Aeromonas and constituent LPS and upregulates the levels of Lachnospiraceae_NK4A136 and butyrate in the colon. These changes lessen the inflammatory response and neuronal apoptosis in the hippocampus through crosstalk between the TLR4/NF-κB and MCT1/ HDAC3 signaling pathways. Video Abstract Supplementary Information The online version contains supplementary material available at 10.1186/s40168-022-01452-3.

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A brief period of sleep deprivation leads to subtle changes in mouse gut microbiota.

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A brief period of sleep deprivation leads to subtle changes in mouse gut microbiota.

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