Prolonged sleep deprivation induces a cytokine-storm-like syndrome in mammals

Sang, Di; Lin, Keteng; Yang, Yini; Ran, Guangdi; Li, Bohan; Chen, Chen; Li, Qi; Ma, Yan; Lu, Lihui; Cui, Xi-Yang; Liu, Zhibo; Lv, Sheng-Qing; Luo, Minmin; Liu, Qinghua; Li, Yulong; Zhang, Eric Erquan

doi:10.1016/j.cell.2023.10.025

Cited by 30 publications

(19 citation statements)

References 110 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As animals have a homeostatic mechanism that drives robust recovery after an initial loss of sleep [ 59 , 60 ], we found that 48 h SR could significantly suppress all phases of sleep and cause hyperalgesia. What’ more, the 48-h SR could not cause mice die with clear environment and this is consistent with Sang’s work [ 40 ]. Although the mice were not completely sleep abolished, they were able to stay in sleep loss for a period.…”

Section: Discussionsupporting

confidence: 90%

“…Sleep loss may cause the accumulation of proinflammatory cytokines in blood and this may be cause by Enhanced efflux through the BBB [ 40 ]. Our previous study found that SR-induced hyperalgesia is associated with the inflammation of the spinal dorsal cord [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…In the current investigation, we used the 48 h SR model as an acute sleep loss model. Acute sleep loss means that individuals remain awake for a short period of time (usually 24 - 72 hours) [ 30 , 40 , 59 ]. As animals have a homeostatic mechanism that drives robust recovery after an initial loss of sleep [ 59 , 60 ], we found that 48 h SR could significantly suppress all phases of sleep and cause hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

“…Although the mice were not completely sleep abolished, they were able to stay in sleep loss for a period. Of course, a more efficient experimental paradigm for continuous SD is necessary to explored [ 40 ]. The in vivo regulatory effect of the mTOR signaling pathway and Tregs depletion in SR mice, however, was not performed due to the challenges in isolating epithelial cells of the spinal cord and cultivating tool mice in a short period.…”

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia

Huang,

Xu,

Liu

et al. 2024

BMC Med

View full text Add to dashboard Cite

Background Sleep loss is a common public health problem that causes hyperalgesia, especially that after surgery, which reduces the quality of life seriously. Methods The 48-h sleep restriction (SR) mouse model was created using restriction chambers. In vivo imaging, transmission electron microscopy (TEM), immunofluorescence staining and Western blot were performed to detect the status of the blood-spinal cord barrier (BSCB). Paw withdrawal mechanical threshold (PWMT) was measured to track mouse pain behavior. The role of infiltrating regulatory T cells (Tregs) and endothelial cells (ECs) in mouse glycolysis and BSCB damage were analyzed using flow cytometry, Western blot, CCK-8 assay, colorimetric method and lactate administration. Results The 48-h SR made mice in sleep disruption status and caused an acute damage to the BSCB, resulting in hyperalgesia and neuroinflammation in the spinal cord. In SR mice, the levels of glycolysis and glycolysis enzymes of ECs in the BSCB were found significantly decreased [CON group vs. SR group: CD31+Glut1+ cells: p < 0.001], which could cause dysfunction of ECs and this was confirmed in vitro. Increased numbers of infiltrating T cells [p < 0.0001] and Treg population [p < 0.05] were detected in the mouse spinal cord after 48-h SR. In the co-cultured system of ECs and Tregs in vitro, the competition of Tregs for glucose resulted in the glycolysis disorder of ECs [Glut1: p < 0.01, ENO1: p < 0.05, LDHα: p < 0.05; complete tubular structures formed: p < 0.0001; CCK8 assay: p < 0.001 on 24h, p < 0.0001 on 48h; glycolysis level: p < 0.0001]. An administration of sodium lactate partially rescued the function of ECs and relieved SR-induced hyperalgesia. Furthermore, the mTOR signaling pathway was excessively activated in ECs after SR in vivo and those under the inhibition of glycolysis or co-cultured with Tregs in vitro. Conclusions Affected by glycolysis disorders of ECs due to glucose competition with infiltrating Tregs through regulating the mTOR signaling pathway, hyperalgesia induced by 48-h SR is attributed to neuroinflammation and damages to the barriers, which can be relieved by lactate supplementation.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia

Huang,

Xu,

Liu

et al. 2024

BMC Med

View full text Add to dashboard Cite

show abstract

“…For the rats’ states (sleep, wake, and walk), the difficulty lies in the judgement of the sleep state. According to current studies, both the rat and mice adopt a curled-up position with lowered heads when they enter the sleep state 60 . In addition, in the bright environments, rats tend to curled-up and sleep with their eyes closed, while in the dark environments, they tend to sleep with their eyes open.…”

Section: Technical Validationmentioning

confidence: 90%

A longitudinal electrophysiological and behavior dataset for PD rat in response to deep brain stimulation

Wang,

Chen,

Shen

et al. 2024

Sci Data

View full text Add to dashboard Cite

Here we presented an electrophysiological dataset collected from layer V of the primary motor cortex (M1) and the corresponding behavior dataset from normal and hemi-parkinson rats over 5 consecutive weeks. The electrophysiological dataset was constituted by the raw wideband signal, neuronal spikes, and local field potential (LFP) signal. The open-field test was done and recorded to evaluate the behavior variation of rats among the entire experimental cycle. We conducted technical validation of this dataset through sorting the spike data to form action potential waveforms and analyzing the spectral power of LFP data, then based on these findings a closed-loop DBS protocol was developed by the oscillation activity response of M1 LFP signal. Additionally, this protocol was applied to the hemi-parkinson rat for five consecutive days while simultaneously recording the electrophysiological data. This dataset is currently the only publicly available dataset that includes longitudinal closed-loop DBS recordings, which can be utilized to investigate variations of neuronal activity within the M1 following long-term closed-loop DBS, and explore additional reliable biomarkers.

show abstract

The influence of sleep disorders on perioperative neurocognitive disorders among the elderly: A narrative review

Chen,

Zhai,

Lan

et al. 2024

Ibrain

View full text Add to dashboard Cite

This review comprehensively assesses the epidemiology, interaction, and impact on patient outcomes of perioperative sleep disorders (SD) and perioperative neurocognitive disorders (PND) in the elderly. The incidence of SD and PND during the perioperative period in older adults is alarmingly high, with SD significantly contributing to the occurrence of postoperative delirium. However, the clinical evidence linking SD to PND remains insufficient, despite substantial preclinical data. Therefore, this study focuses on the underlying mechanisms between SD and PND, underscoring that potential mechanisms driving SD‐induced PND include uncontrolled central nervous inflammation, blood–brain barrier disruption, circadian rhythm disturbances, glial cell dysfunction, neuronal and synaptic abnormalities, impaired central metabolic waste clearance, gut microbiome dysbiosis, hippocampal oxidative stress, and altered brain network connectivity. Additionally, the review also evaluates the effectiveness of various sleep interventions, both pharmacological and nonpharmacological, in mitigating PND. Strategies such as earplugs, eye masks, restoring circadian rhythms, physical exercise, noninvasive brain stimulation, dexmedetomidine, and melatonin receptor agonists have shown efficacy in reducing PND incidence. The impact of other sleep‐improvement drugs (e.g., orexin receptor antagonists) and methods (e.g., cognitive‐behavioral therapy for insomnia) on PND is still unclear. However, certain drugs used for treating SD (e.g., antidepressants and first‐generation antihistamines) may potentially aggravate PND. By providing valuable insights and references, this review aimed to enhance the understanding and management of PND in older adults based on SD.

show abstract

Prolonged sleep deprivation induces a cytokine-storm-like syndrome in mammals

Cited by 30 publications

References 110 publications

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia

A longitudinal electrophysiological and behavior dataset for PD rat in response to deep brain stimulation

The influence of sleep disorders on perioperative neurocognitive disorders among the elderly: A narrative review

Contact Info

Product

Resources

About