Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep

Shoham, Shai; Davenne, Damien; Cady, Alan B.; Dinarello, Charles A.; Krueger, James M.

doi:10.1152/ajpregu.1987.253.1.r142

Cited by 148 publications

(130 citation statements)

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“…Consistent with current results, they affect each other's production and inhibition of one attenuates the sleep induced by the other (Takahashi et al, 1999. Low doses of IL1β or TNFα enhance non rapid eye movement sleep (NREMS) (Kapas et al, 1992;Krueger et al, 1984;Shoham et al, 1987;Tobler et al, 1984). Conditions associated with increases in endogenous levels of IL1β or TNFα, e.g., time-of-day (Floyd and Krueger, 1997;Taishi et al, 1998), excessive food intake or infectious disease (Toth and Krueger, 1988) promote NREMS.…”

Section: Discussionsupporting

confidence: 73%

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: Discussionsupporting

confidence: 73%

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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“…The mechanisms through which cytokines influence delta power during NREMS are complex and not fully understood. Early studies (28,39,49,52) demonstrate that cytokines alter EEG parameters and that these effects depend on the dose, time, and route of administration. For example, central administration of TNF enhances delta power during NREM sleep (50,51), whereas intraperitoneal administration increases NREM sleep duration without a concomitant increase of EEG delta power (15,16,27,51).…”

Section: Discussionmentioning

confidence: 99%

Sepsis-induced alterations in sleep of rats

Baracchi

Ingiosi²,

Raymond³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Sepsis is a systemic immune response to infection that may result in multiple organ failure and death. Polymicrobial infections remain a serious clinical problem, and in the hospital, sepsis is the number-one noncardiac killer. Although the central nervous system may be one of the first systems affected, relatively little effort has been made to determine the impact of sepsis on the brain. In this study, we used the cecal ligation and puncture (CLP) model to determine the extent to which sepsis alters sleep, the EEG, and brain temperature (Tbr) of rats. Sepsis increases the amount of time rats spend in non-rapid eye movement sleep (NREMS) during the dark period, but not during the light period. Rapid eye movements sleep (REMS) of septic rats is suppressed for about 24 h following CLP surgery, after which REMS increases during dark periods for at least three nights. The EEG is dramatically altered shortly after sepsis induction, as evidenced by reductions in slow-frequency components. Furthermore, sleep is fragmented, indicating that the quality of sleep is diminished. Effects on sleep, the EEG, and Tbr persist for at least 84 h after sepsis induction, the duration of our recording period. Immunohistochemical assays focused on brain stem mechanisms responsible for alterations in REMS, as little information is available concerning infection-induced suppression of this sleep stage. Our immunohistochemical data suggest that REMS suppression after sepsis onset may be mediated, in part, by the brain stem GABAergic system. This study demonstrates for the first time that sleep and EEG patterns are altered during CLP-induced sepsis. These data suggest that the EEG may serve as a biomarker for sepsis onset. These data also contribute to our knowledge of potential mechanisms, whereby infections alter sleep and other central nervous system functions. thermoregulation; behavior; cytokines; circadian rhythms; cecal ligation and puncture SEPSIS RESULTS FROM AN AMPLIFIED inflammatory response to an infectious process that leads to organ dysfunction or risk for secondary infection. As a clinical syndrome, sepsis is defined by the presence of infection and a systemic inflammatory response (7,29). In spite of the ever-increasing sophistication of our antimicrobial armamentarium, sepsis continues to kill millions of people worldwide, and the diagnosis of sepsis still confers a 20 -50% risk of mortality (1, 33). The National Center for Health Statistics now lists sepsis among the top 10 leading causes of death in the United States, and, in fact, sepsis/septic shock is the leading cause of death among patients in noncoronary hospital units (34,48). For those who survive, the impact of severe sepsis does not end with hospital discharge. Mortality from all causes increases from 21% at admission to ϳ75% five years after index admission for severe sepsis (60). Furthermore, survivors of sepsis often suffer from new, persistent, and dramatic cognitive impairment (25). These epidemiologic data demonstrate that sepsis must also be viewed as ...

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“…IL-1β increases the amplitude of EEG slow waves during NREMS in rabbit and rat, but these changes are dependent on the dose and on the time of administration (Shoham et al, 1987;Opp et al, 1991). Whereas central administration of TNFα enhances slow wave oscillations during NREMS (Takahashi et al, 1996c(Takahashi et al, , 1997, intraperitoneal injection of TNFα increases NREMS duration without a concomitant increase of EEG delta power Kubota et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

Baracchi¹,

Opp²

2008

Brain, Behavior, and Immunity

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Data indicate that interleukin (IL)-1β and tumor necrosis factor-α (TNFα) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1β type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFα spend less time in NREMS during the dark period. To further investigate roles for IL-1β and TNFα in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1β receptor 1 and TNFα receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n = 14; B6129SF2/J, n = 14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6 h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6 h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1β and TNFα cytokine systems play a role in sleep regulation and in the alterations in sleep that follow prolonged wakefulness.

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Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep

Cited by 148 publications

References 0 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

Sepsis-induced alterations in sleep of rats

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

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