Soluble TNF-α receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight

Shearer, William T.; Reuben, James M.; Mullington, Janet; Price, Nicholas J.; Lee, Bang Ning; Smith, E. O’Brian; Szuba, Martin P.; Dongen, Hans P A Van; Dinges, David F.

doi:10.1067/mai.2001.112270

Cited by 409 publications

(262 citation statements)

References 33 publications

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“…IL1β increases the firing rate of a subpopulation of anterior hypothalamic, sleep-active neurons while it suppresses the firing rate in most of the wake-active neurons in this region (Alam et al, 2004). Other cytokines, such as interleukin-6 and interleukin-10 ( Alberti et al, 2003;Hogan et al, 2003;Toth and Opp, 2001;Shearer et al, 2001;Smith et al, 1999) as well as NGF (Kapas et al, 1996) and BDNF , also affect sleep and interact with TNFα and IL1β. Current results have bearing on these findings to the extent that we demonstrate that both IL1 and TNF have broad-ranging actions on other cytokines; each with distinct time courses of mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

Cytokine mRNA induction by interleukin-1β or tumor necrosis factor α in vitro and in vivo

Taishi

Churchill

et al. 2008

Brain Research

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Hypothalamic and cortical mRNA levels for cytokines such as interleukin-1α (IL1α), tumor necrosis factor alpha (TNFα), nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) are impacted by systemic treatments of IL1β and TNFα To investigate the time course of the effects of IL1β and TNFα on hypothalamic and cortical cytokine gene expression, we measured mRNA levels for IL1β, TNFα, interleukin-6 (IL-6), interleukin-10 (IL-10), IL1 receptor 1, BDNF, NGF, and glutamate decarboxylase-67 in vitro using hypothalamic and cortical primary cultures. IL1β and TNFα mRNA levels increased significantly in a dose-dependent fashion after exposure to either IL1β or TNFα. IL1β increased IL1β mRNA in both the hypothalamic and cortical cultures after 2-6 h while TNFα mRNA increased significantly within 30 min and continued to rise up to 2-6 h. Most of the other mRNAs showed significant changes independent of dose in vitro. In vivo, intracerebroventricular (icv) injection of IL1β or TNFα also significantly increased IL1β, TNFα and IL6 mRNA levels in the hypothalamus and cortex. IL1β icv, but not TNFα increased NGF mRNA levels in both these areas. Results support the hypothesis that centrally active doses of IL1β and TNFα enhance their own mRNA levels as well as affect mRNA levels for other neuronal growth factors.

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Section: Discussionmentioning

confidence: 99%

Cytokine mRNA induction by interleukin-1β or tumor necrosis factor α in vitro and in vivo

Taishi

Churchill

et al. 2008

Brain Research

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“…Similarly, sleep deprivation has been associated with a number of potentially relevant deleterious effects on brain homeostasis, including changes in brain temperature [31], glutamate concentrations [32], and energy consumption as evidenced by decreased levels of brain glycogen [33]. Sleep deprivation also results in elevated proinflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α), which can impair neuronal growth and delay recovery [34,35]. If sleep loss incurs these neurophysiologic costs and also impairs neurorecovery, it is reasonable to hypothesize that postinjury sleep enhancement may facilitate neurorecovery.…”

Section: Essential Questions Related To Mtbi and Sleep Why Does Sleepmentioning

confidence: 99%

Sleep, Sleep Disorders, and Mild Traumatic Brain Injury. What We Know and What We Need to Know: Findings from a National Working Group

et al. 2016

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Disturbed sleep is one of the most common complaints following traumatic brain injury (TBI) and worsens morbidity and long-term sequelae. Further, sleep and TBI share neurophysiologic underpinnings with direct relevance to recovery from TBI. As such, disturbed sleep and clinical sleep disorders represent modifiable treatment targets to improve outcomes in TBI. This paper presents key findings from a national working group on sleep and TBI, with a specific focus on the testing and development of sleep-related therapeutic interventions for mild TBI (mTBI). First, mTBI and sleep physiology are briefly reviewed. Next, essential empirical and clinical questions and knowledge gaps are addressed. Finally, actionable recommendations are offered to guide active and efficient collaboration between academic, industry, and governmental stakeholders.

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“…Increased daytime plasma levels of IL-6 were also noted after sleep deprivation and in patients with excessive daytime sleepiness. 4,14,20 IL-6 is one of the key regulators of CRP synthesis by the liver. 5 The repetitive apneas during OSA induce not only hypoxemia, but also sleep fragmentation with consequent insufficient sleep and daytime somnolence.…”

Section: Shamsuzzaman Et Al Obstructive Sleep Apnea and C-reactive Prmentioning

confidence: 99%

Elevated C-Reactive Protein in Patients With Obstructive Sleep Apnea

et al. 2002

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Background-Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular and cerebrovascular disease.Inflammatory processes associated with OSA may contribute to cardiovascular morbidity in these patients. We tested the hypothesis that OSA patients have increased plasma C-reactive protein (CRP). Methods and Results-We studied 22 patients (18 males and 4 females) with newly diagnosed OSA, who were free of other diseases, had never been treated for OSA, and were taking no medications. We compared CRP measurements in these patients to measurements obtained in 20 control subjects (15 males and 5 females) who were matched for age and body mass index, and in whom occult OSA was excluded. Plasma CRP levels were significantly higher in patients with OSA than in controls (median Epidemiological studies show that an elevated CRP level in the high-normal (0.2 to 1.5 mg/dL) range in apparently healthy men and women is a strong predictor of cardiovascular risk. 7,8 In patients with acute coronary artery disease, stable angina pectoris, and a history of myocardial infarction, higher CRP is also associated with future cardiovascular events. 9 10 OSA results in repetitive and severe nocturnal hypoxemia and sleep disturbances. 11 The hypoxemia of high altitude results in increases in interleukin-6 (IL-6) 12 and CRP 12,13 in normal humans. Sleep deprivation also induces an increase in cytokines. 4,14 We tested the hypothesis that OSA patients have increased plasma CRP. MethodsWe compared subjects with moderate to severe OSA (apnea hypopnea index [AHI] Ն20) to those without OSA (AHI Յ5). We studied 22 patients (18 males and 4 females) with newly diagnosed OSA, who were free of other diseases, had never been treated for OSA, and were taking no medications. We compared CRP measurements in these patients to measurements obtained from 20 control subjects (15 males and 5 females) who were matched for age and body mass index (BMI), and in whom occult OSA was excluded. The control group was free of any acute or chronic cardiovascular, inflammatory, or sleep disorders, and no control subjects were taking medications at the time of the sleep study. The presence and severity of sleep apnea were determined by standard overnight polysomnography, including electroencephalography, electrooculography, electromyography, oximetry, thermistor measurements of airflow, and measurements of rib cage and abdominal movements when breathing. The sleep studies followed a split-night protocol. The first half of the study intended to diagnose OSA, with a therapeutic trial of continuous positive airway pressure during the second half of the night. An apnea was defined as complete cessation of airflow for at least 10 seconds. Hypopnea was defined as a reduction of respiratory signals for at least 10 seconds associated with oxygen desaturation of Ն4%. The AHI was calculated as the total number of respiratory events per hour of sleep.Baseline demographic data, heart rate, blood pressure (SpaceLabs blood pressure monitor 90207), and venous blood ...

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Soluble TNF-α receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight

Cited by 409 publications

References 33 publications

Cytokine mRNA induction by interleukin-1β or tumor necrosis factor α in vitro and in vivo

Cytokine mRNA induction by interleukin-1β or tumor necrosis factor α in vitro and in vivo

Sleep, Sleep Disorders, and Mild Traumatic Brain Injury. What We Know and What We Need to Know: Findings from a National Working Group

Elevated C-Reactive Protein in Patients With Obstructive Sleep Apnea

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