Effects of i.c.v. administration of interleukin-1 on sleep and body temperature of interleukin-6-deficient mice

Olivadoti, Melissa; Opp, Mark R.

doi:10.1016/j.neuroscience.2008.02.008

Cited by 48 publications

(46 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several cytokines (IL-1␤, IL-6) and chemokines (MIP-1␣, MIP-1␤) act as endogenous pyrogens in the hypothalamus during bacterial infection. For example, direct injection of IL-1␤ into the brain increases body temperature and non-REM sleep (28). Furthermore, IL-1 mRNA and protein are synthesized in the hypothalamus in response to peripheral pyrogenic stimuli such as LPS (15,24) as well as HS (22).…”

Section: Discussionmentioning

confidence: 99%

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Biedenkapp¹,

Leon

2013

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Biedenkapp JC, Leon LR. Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery. Am J Physiol Regul Integr Comp Physiol 305: R978 -R986, 2013. First published September 11, 2013 doi:10.1152/ajpregu.00011.2013.-Heat stroke (HS) is characterized by a systemic inflammatory response syndrome (SIRS) consisting of profound core temperature (Tc) changes in mice. Encephalopathy is common at HS collapse, but inflammatory changes occurring in the brain during the SIRS remain unidentified. We determined the association between inflammatory gene expression changes in the brain with Tc disturbances during HS recovery in mice. Gene expression changes of heat shock protein (HSP)72, heme oxygenase (hmox1), cytokines (IL-1␤, IL-6, TNF-␣), cyclooxygenase enzymes (COX-1, COX-2), chemokines (MCP-1, MIP-1␣, MIP-1␤, CX 3CR1), and glia activation markers (CD14, aif1, vimentin) were examined in the hypothalamus (HY) and hippocampus (HC) of control (Tc ϳ 36.0°C) and HS mice at Tc,Max (42.7°C), hypothermia depth (HD; 29.3 Ϯ 0.4°C), and fever (37.8 Ϯ 0.3°C). HSP72 (HYϽHC) and IL-1␤ (HY only) were the only genes that showed increased expression at Tc,Max. HSP72 (HY Ͻ HC), hmox1 (HY Ͻ HC), cytokine (HY ϭ HC), and chemokine (HY ϭ HC) expression was highest at HD and similar to controls during fever. COX-1 expression was unaffected by HS, whereas HD was associated with approximately threefold increase in COX-2 expression (HY only). COX-2 expression was not increased during fever and indomethacin (COX inhibitor) had no effect on this Tc response indicating fever is regulated by other inflammatory pathways. CD14, aif1, and vimentin activation at HD coincided with maximal cytokine and chemokine expression suggesting glia cells are a possible source of brain cytokines and chemokines during HS recovery. The inflammatory gene expression changes during HS recovery suggest cytokines and/or chemokines may be initiating development or rewarming from hypothermia, whereas fever pathway(s) remain to be elucidated. heat stroke; cytokines; chemokines; hypothermia; fever; systemic inflammatory response HEAT STROKE (HS) is a serious form of hyperthermia characterized by a systemic inflammatory response syndrome (SIRS) leading to multiorgan dysfunction in which encephalopathy (e.g., ataxia, delirium, coma) predominates (5). The most common central nervous system (CNS) disturbance in HS patients is cerebellar dysfunction, which manifests as ataxia at the time of collapse (5,25,26). Postmortem analysis of HS victims showed histological damage and glia proliferation in the cerebellum that appeared to be the pathological basis for motor sequelae observed upon clinical admission (25). However, not all pathophysiological responses associated with the SIRS show a direct correlate to brain regions that experience cellular damage with HS. For example, HS patients and animal models often display core temperature (T c ) disturbances (e.g., hypothermia, fever) during recovery that occur in the absence of damage to the preoptic ante...

show abstract

Section: Discussionmentioning

confidence: 99%

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Biedenkapp¹,

Leon

2013

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Administration of these cytokines to rodents results in increased time spent asleep, and, conversely, cytokine antagonists have the opposite effects (44,73). Elevated levels of TNF␣ and IL-6 have also been reported in patients with sleep disorders such as narcolepsy and sleep apnea, which are commonly associated with increased daytime sleepiness (104).…”

Section: Sleep Disturbances and Liver Diseasementioning

confidence: 99%

Liver-brain inflammation axis

D’Mello

Swain

2011

American Journal of Physiology-Gastrointestinal and Liver Physi

105

View full text Add to dashboard Cite

It is becoming increasingly evident that peripheral organ-centered inflammatory diseases, including chronic inflammatory liver diseases, are associated with changes in central neural transmission that result in alterations in behavior. These behavioral changes include sickness behaviors, such as fatigue, cognitive dysfunction, mood disorders, and sleep disturbances. While such behaviors have a significant impact on quality of life, the changes within the brain and the communication pathways between the liver and the brain that give rise to changes in central neural activity are not fully understood. Traditionally, neural and humoral communication pathways have been described, with the three cytokines TNFα, IL-1β, and IL-6 receiving the most attention in mediating communication between the periphery and the brain, in the setting of peripheral inflammation. However, more recently, we described an immune-mediated communication pathway in experimentally induced liver inflammation whereby, in response to activation of resident immune cells in the brain (i.e., the microglia), peripheral circulating monocytes transmigrate into the brain, leading to development of sickness behaviors. These signaling pathways drive changes in behavior by altering central neurotransmitter systems. Specifically, changes in serotonergic and corticotropin-releasing hormone neurotransmission have been demonstrated and implicated in liver inflammation-associated sickness behaviors. Understanding how the liver communicates with the brain in the setting of chronic inflammatory liver diseases will help delineate novel therapeutic targets that can reduce the burden of symptoms in patients with liver disease.

show abstract

“…(Irwin and others 2006;Mills and others 2007). Administration of any of these cytokines increases the time spent in non-REM sleep (Olivadoti andOpp 2008). 2001).…”

Section: Introductionmentioning

confidence: 99%

REM Sleep Deprivation in Rats Results in Inflammation and Interleukin-17 Elevation

Yehuda

Sredni

Carasso

et al. 2009

Journal of Interferon & Cytokine Research

130

View full text Add to dashboard Cite

Sleep deprivation is a major health problem in modern society. Deprivation of rapid eye movement (REM) sleep is particularly damaging to cognition and to spatial memory; however, the mechanisms that mediate these deteriorations in function are not known. We explored the possibility that REM sleep deprivation may provoke major changes in the immune system by inducing inflammation. Rats were subjected to 72 h of REM sleep deprivation, and the plasma levels of proinflammatory cytokines (IL-1, IL-1beta, IL-6, IL-17A, and TNF-alpha), an anti-inflammatory cytokine (IL-10), the inflammatory markers homocysteine, corticosterone, and hyperthermia were measured immediately after the deprivation period, and 7 days later. The results indicate that REM sleep deprivation induced an inflammatory response. The levels of the proinflammatory cytokines and markers were significantly elevated in sleep-deprived rats as compared to control rats. After 7 days of recovery, the levels of some markers, including hyperthermia, remained higher in sleep-deprived rats versus the control animals. IL-17A appears to play a pivotal role in coordinating the inflammation. These data shed new light on the mechanism of sleep deprivation-induced inflammation.

show abstract

Effects of i.c.v. administration of interleukin-1 on sleep and body temperature of interleukin-6-deficient mice

Cited by 48 publications

References 53 publications

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Liver-brain inflammation axis

REM Sleep Deprivation in Rats Results in Inflammation and Interleukin-17 Elevation

Contact Info

Product

Resources

About