Sleep and Cerebrospinal Fluid Interleukin-1-Like Activity in the Cat

Fa, Lue; M, Bail; J, Jephthah-Ochola; Carayanniotis, Karen A.; Gorczynski, Reg; Moldofsky, Harvey

doi:10.3109/00207458808991595

Cited by 101 publications

(33 citation statements)

References 9 publications

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“…Since the cytokine production increased shortly before sleep onset and since IL-1P has previously been shown to exhibit somnogenic effects, our data may indicate that cytokines participate in the physiological regulation of sleep. Our findings are in line with results reported by Moldofsky et al [13] and are supported by animal experiments describingan elevation of IL-1-like biological activity in the cere brospinal fluid of cats while asleep as compared to wake fulness [ 18]. Nevertheless, the question still remains open whether the observed periodicity of cytokines and cortisol is related to the sleep-wake cycle, whether it is a conse quence of motor activity and bedrest or whether it is a true circadian rhythm.…”

Section: Discussionsupporting

confidence: 80%

Cytokine Production during Sleep and Wakef ulness and Its Relationship to Cortisol in Healthy Humans

et al. 1993

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A growing body of evidence indicates that cytokines, especially interleukin-1 β, are involved in the regulation of sleep and wakefulness. The aim of the present pilot study was to investigate the relationship between interleukin-lβ (IL-lβ) and γ-interferon (γ-IFN) production and the regulation of sleep and wakefulness. Four healthy male volunteers were investigated. After one adaptation night, beginning at 8 a.m. in the morning, the EEG was recorded by means of a mobile long-term EEG and blood samples were drawn every 45 min for the analysis of IL-lβ, γ-IFN and cortisol for 24 h. For the analysis of cytokines whole blood cultures were established. After 48 h of incubation in the presence of endotoxin Salmonella typhimurium, IL-lβ and γ-IFN levels were measured in the culture supernatants using specific immunodetection assays. Methods of stochastic time series analysis were adopted to evaluate the biochemical data. Our results show the capability of cultered blood cells to produce cytokines upon endotoxin challenge to be at a maximum around the time of sleep onset and during the first hours of sleep, declining during the night to a minimum level in the morning hours. The opposite was observed for cortisol. The analysis of autocorrelation functions gives evidence of a 24-hour rhythm of cortisol and cytokines. The results indicate that the cytokines IL-1 β and γ-IFN may play a role in sleep regulation.

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Section: Discussionsupporting

confidence: 80%

Cytokine Production during Sleep and Wakef ulness and Its Relationship to Cortisol in Healthy Humans

et al. 1993

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“…IL-1 and TNF mRNA have diurnal rhythms in brain with the highest values being associated with periods of maximum sleep. TNF protein also has a sleep-associated diurnal rhythm in several brain areas and IL-1in cerebrospinal fluid varies with the sleep-wake cycle (Lue et al, 1988).…”

Section: Animal Modelsmentioning

confidence: 99%

Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Irwin

Opp

2016

Neuropsychopharmacol

364

268

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Sleep disturbances including insomnia independently contribute to risk of inflammatory disorders and major depressive disorder. This review and overview provides an integrated understanding of the reciprocal relationships between sleep and the innate immune system and considers the role of sleep in the nocturnal regulation of the inflammatory biology dynamics; the impact of insomnia complaints, extremes of sleep duration, and experimental sleep deprivation on genomic, cellular, and systemic markers of inflammation; and the influence of sleep complaints and insomnia on inflammaging and molecular processes of cellular aging. Clinical implications of this research include discussion of the contribution of sleep disturbance to depression and especially inflammation-related depressive symptoms. Reciprocal action of inflammatory mediators on the homeostatic regulation of sleep continuity and sleep macrostructure, and the potential of interventions that target insomnia to reverse inflammation, are also reviewed. Together, interactions between sleep and inflammatory biology mechanisms underscore the implications of sleep disturbance for inflammatory disease risk, and provide a map to guide the development of treatments that modulate inflammation, improve sleep, and promote sleep health.

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“…Inhibition of IL-1 by the IL-1RA or by antibodies suppresses spontaneous sleep [reviewed in 21. Finally, IL-1 concentration in the cerebrospinal fluid varies with the sleep-wake cycle [7]. Collectively, these observations suggest that intracerebral IL-1 is, in fact, a physiological sleep factor.…”

Section: Is Il-1 Involved In Normal Sleep Regulation?mentioning

confidence: 70%

Hypothalamic releasing hormones mediating the effects of interleukin‐1 on sleep

Payne

Obál

Krueger

1993

J of Cellular Biochemistry

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There is a substantial literature describing the interactions between the endocrine and immune systems. Although such interactions are less well known within the brain, one major brain function altered during inflammation and infection and by several endocrine hormones is sleep. Pathological disturbances, be they inflammation, infectious disease, and/or sleep deprivation, result in altered hypothalamus-pituitary function and cytokine metabolism. In respect to hormone secretion from the pituitary, cytokines are now recognized to play an important role in modulating the neuroendocrine system. Changes in sleep provide a useful illustration of the interactions between cytokines and the hypothalamus-pituitary axis. Evidence linking interleukin-I (IL-I ) to growth hormone releasing hormone and to corticotropin releasing hormone in regard to their effects on sleep is reviewed. c 1993 WiIey-Liss, Inc.Key words: cytokines, growth hormone releasing hormone, corticotropin releasing hormone, endocrine regulation, neuroendocrineThe host's initial response to infections is a nonspecific defense reaction called the acute phase response. The acute phase response promotes specific responses to the infectious agents mediated by cellular and humoral immune mechanisms. The acute phase response does this by several ways: the immune system is stimulated; an environment is provided which enhances the effectiveness of the specific immune response and at the same time is not optimal for the replication and spreading of the infectious agents; and the behavior and responsiveness to stimuli of the individual are modified in such a way that the exposure to further environmental challenges is reduced. These changes require substantial alterations in almost all functions of the body. The clinical manifestations of these alterations are the leading symptoms of sickness which are easily recognized by everybody: fever, somnolence, social withdrawal, reduced apetite, muscle pain, etc. Laboratory readings are also abnormal; changes are recorded in plasma proteins, in the number Received May 17, 1993; accepted July 16, 1993. Address reprint requests to James M. Krueger, University of Tennessee, Department of Physiology and Biophysics, 894 Union Avenue, Memphis, TN 38163. and percentage distribution of leukocytes, and in concentrations of various hormones: red blood cell sedimentation increases, and the basal metabolic rate is elevated [ll. An acute phase response, exaggerated in magnitude or prolonged, is detrimental to the individual. However, negative feedback mechanisms are also activated which attenuate various aspects of the functional changes and abolish the response when the infection is eliminated.Much information has accumulated within the past few years indicating that most, if not all, aspects of the acute phase response are driven by a complex array of cytokines in association with classical stress hormones [21. Most cytokines were first identified as immunocyte products involved in the amplification, coordination, and regulatio...

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Sleep and Cerebrospinal Fluid Interleukin-1-Like Activity in the Cat

Abstract: Exogenous interleukin-1 (IL-1), applied intraventricularly, has been reported to enhance slow wave sleep. Here, we demonstrate that endogenous interleukin-1-like activity and IL-1 beta of the cat CSF increases during sleep in comparison to wake.

Cited by 101 publications

References 9 publications

Cytokine Production during Sleep and Wakef ulness and Its Relationship to Cortisol in Healthy Humans

Cytokine Production during Sleep and Wakef ulness and Its Relationship to Cortisol in Healthy Humans

Sleep Health: Reciprocal Regulation of Sleep and Innate Immunity

Hypothalamic releasing hormones mediating the effects of interleukin‐1 on sleep

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