scholarly journals Sleep-promoting effects of endogenous pyrogen (interleukin-1)

1984 ◽  
Vol 246 (6) ◽  
pp. R994-R999 ◽  
Author(s):  
J. M. Krueger ◽  
J. Walter ◽  
C. A. Dinarello ◽  
S. M. Wolff ◽  
L. Chedid
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Interleukin 1 ◽  
Cerebral Ventricles ◽  
Endogenous Pyrogen ◽  
Temperature Heating ◽  
Dose Dependent ◽  
Pyrogenic Activity

When infused into the lateral cerebral ventricles of rabbits, human endogenous pyrogen (EP) preparations induced dose-dependent increases in slow-wave sleep concomitant with increasing body temperature. Heating EP to 70 degrees C destroyed its sleep-promoting and pyrogenic activity. Anisomycin (an antipyretic) prevented EP from increasing body temperature without affecting its sleep-promoting activity. Intravenous injection of EP induced fever and transient increases in slow-wave sleep but failed to induce prolonged increases in slow-wave sleep. We conclude that the somnogenic activity of EP is not secondary to its pyrogenic activity.

Body temperature response to IL-1 beta in pregnant rats

1995 ◽  
Vol 269 (5) ◽  
pp. R1179-R1182 ◽  
Author(s):  
R. L. Simrose ◽  
J. E. Fewell
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Interleukin 1 ◽  
Temperature Response ◽  
Sprague Dawley ◽  
Endogenous Pyrogen ◽  
Febrile Response ◽  
Pregnant Rats ◽  
Sprague Dawley Rats ◽  
Near Term

Rats have an attenuated or absent febrile response to exogenous pyrogen (e.g., bacterial endotoxin) near term of pregnancy. With the aim of providing insight into possible mechanism(s) of the altered febrile response to exogenous pyrogen, experiments have been carried out on 67 time-bred Sprague-Dawley rats to investigate the febrile response to endogenous pyrogen [i.e., interleukin-1 beta (IL-1 beta)]. On day 13 of gestation, intravenous injection of IL-1 beta produced a significant increase in body temperature with a latency of approximately 30 min and a duration of approximately 120 min. In contrast, on days 17 and 21 of gestation as well as on the day of delivery, intravenous injection of IL-1 beta produced significant decreases in body temperature. Thus rats do not develop fever in response to endogenous pyrogen near term of pregnancy but rather become hypothermic. The mechanism of the altered body temperature response to exogenous pyrogen as pregnancy proceeds remains unknown. We speculate, however, that it most likely lies downstream from the formation of endogenous pyrogen.

Indomethacin blocks the febrile response induced by interleukin-8 in rabbits

1995 ◽  
Vol 269 (6) ◽  
pp. R1469-R1474 ◽  
Author(s):  
A. R. Zampronio ◽  
C. A. Silva ◽  
F. Q. Cunha ◽  
S. H. Ferreira ◽  
I. R. Pela ◽  
...  
Keyword(s):  
Body Temperature ◽  
Intravenous Injection ◽  
Interleukin 8 ◽  
Intracerebroventricular Injection ◽  
Febrile Response ◽  
Limulus Amoebocyte Lysate ◽  
Intracerebroventricular Injections ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Pyrogenic Activity

Interleukin (IL)-8 induces fever in rats by a mechanism independent of the release of cyclooxygenase products. The purpose of this study was to investigate whether a similar mechanism is responsible for the pyrogenic effect of IL-8 in rabbits. Intravenous (0.31-5.0 ng/kg) or intracerebroventricular (15.6-250 pg) injections of IL-8 induced a dose-dependent increase in body temperature. The correlations between the doses of recombinant human IL-8 and the fever index were 0.98 and 0.99 for the intravenous and intracerebroventricular injections, respectively. The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS), inasmuch as the Limulus amoebocyte lysate test showed < 10 pg endotoxin/micrograms IL-8, and boiled IL-8 lost its pyrogenic activity. Indomethacin (2 and 5 mg/kg i.p.) abolished the febrile response induced by the intravenous injection of LPS (5.0 ng/kg), IL-1 beta (5 ng/kg), and IL-8 (5 ng/kg). Indomethacin also abolished the fever induced by the intracerebroventricular injection of IL-8 (62.5 pg) but only partially reduced the response induced by the injection of IL-1 beta (25 pg icv). These results show that, different from rats, indomethacin blocks the febrile response induced by the central or peripheral administration of IL-8 in rabbits.

Interleukin-8 induces fever by a prostaglandin-independent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. R1670-R1674 ◽  
Author(s):  
A. R. Zampronio ◽  
G. E. Souza ◽  
C. A. Silva ◽  
F. Q. Cunha ◽  
S. H. Ferreira
Keyword(s):  
Body Temperature ◽  
Interleukin 1 ◽  
Interleukin 8 ◽  
Cyclooxygenase Inhibitors ◽  
Interleukin 1 Beta ◽  
Independent Mechanism ◽  
Intracerebroventricular Injections ◽  
Beta 2 ◽  
Dose Dependent ◽  
Pyrogenic Activity

We have studied the mechanism by which interleukin-8 (IL-8) induces fever in rats. Intracerebroventricular injections of IL-8 (5.5-50 ng) evoked dose-dependent increases in body temperature, which reached a plateau 5 h after injection, i.e., later than intracerebroventricular interleukin-1 beta (IL-1 beta; 2 h). The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS) because preincubation of IL-8 with a specific antibody or boiling the IL-8 for 30 min abolished its activity but not that of LPS; also, IL-8 but not LPS induced fever in LPS-tolerant rats. Indomethacin significantly reduced the pyrogenic effects of intracerebroventricular injections of LPS and IL-1 beta but not responses to IL-8, suggesting that pyrogenic responses to IL-8 were mediated independently of prostaglandins. In contrast, dexamethasone markedly attenuated pyrogenic responses to IL-8 and IL-1 beta. These data suggest that inhibition of IL-8 by glucocorticoids contributes to the antipyretic effects of these drugs in fevers resistant to cyclooxygenase inhibitors.

Fever and thermogenesis in response to bacterial endotoxin involve macrophage-dependent mechanisms in rats

1993 ◽  
Vol 265 (5) ◽  
pp. R1179-R1183 ◽  
Author(s):  
R. H. Derijk ◽  
P. J. Strijbos ◽  
N. van Rooijen ◽  
N. J. Rothwell ◽  
F. Berkenbosch
Keyword(s):  
Oxygen Consumption ◽  
Body Temperature ◽  
Intravenous Injection ◽  
Immune Cells ◽  
Interleukin 1 ◽  
Important Mediator ◽  
Selective Elimination ◽  
Colonic Temperature ◽  
Higher Doses ◽  
Intact Rats

Increases in thermogenesis and body temperature (fever) frequently accompany infection or injury and are thought to be mediated by endogenous pyrogens (e.g. cytokines), which are released from activated immune cells such as macrophages. Therefore, we have investigated the effect of selective elimination of peripheral macrophages on the changes in oxygen consumption (VO2) and colonic temperature in response to bacterial lipopolysaccharide (LPS) in the rat. Peripheral macrophages were depleted by intravenous injection of liposomes containing the drug dichloromethylene diphosphonate (Cl2MDP). Resting oxygen consumption and colonic temperatures were not affected by macrophage elimination. In intact rats, peripheral injection of LPS (0.1-0.5 mg/kg) elicited an increase in colonic temperature and in oxygen consumption that declined at higher doses (2.5 mg/kg). The pyrogenic and thermogenic responses to LPS were significantly attenuated in rats in which peripheral macrophages were eliminated. Previously, we have reported that elimination of macrophages blunts the plasma interleukin-1 (IL-1) response to LPS. Here we show that elimination of macrophages does not affect the increase in plasma IL-6 concentrations in response to LPS. These data indicate that the pyrogenic and thermogenic responses to LPS are at least in part dependent on mechanisms involving peripheral macrophages, and that peripherally produced IL-1 rather than IL-6 may be an important mediator of the changes in oxygen consumption and colonic temperature in response to LPS.

Ambulatory Estimation of Circadian Rhythms Shows Core Body Temperature Phase Precedes Slow Wave Sleep Phase in the Normal Elderly

2020 ◽  
Vol 87 (9) ◽  
pp. S251
Author(s):  
Esther Blessing ◽  
Ankit Paresh ◽  
Arleener Turner ◽  
Andrew Varga ◽  
David Rapoport ◽  
...  
Keyword(s):  
Body Temperature ◽  
Circadian Rhythms ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Core Body Temperature ◽  
Temperature Phase ◽  
Sleep Phase ◽  
Core Body

scholarly journals Effects of anti-inflammatory drugs on fever and neutrophilia induced byClostridium difficiletoxin B

1996 ◽  
Vol 5 (3) ◽  
pp. 183-187 ◽  
Author(s):  
R. A. Cardoso ◽  
A. A. Melo Filho ◽  
M. C. C. Melo ◽  
D. M. Lyerly ◽  
T. D. Wilkins ◽  
...  
Keyword(s):  
Body Temperature ◽  
Clostridium Difficile ◽  
Intravenous Injection ◽  
Febrile Response ◽  
Toxin B ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Dose Dependent Increase ◽  
Dose Dependent

This study investigated the ability ofClostridium difficiletoxin B, isolated from the VPI 10463 strain, to induce fever and neutrophilia in rats. Intravenous injection of toxin B (0.005–0.5 μg/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 μg/kg of the toxin started in 2.5 h, peaked at 5 h, and subsided fully within 24 h. Toxin B also induced a dosedependent neutrophilia. Pretreatment with indomethacin (2 mg/kg, i.p.) did not affect the neutrophilia induced by toxin B, but significantly reduced the febrile response measured 4 to 8 h after toxin B injection. Dexamethasone (0.5 mg/ kg) also markedly diminished the febrile response induced by toxin B. These results show thatClostridium difficiletoxin B induced a febrile response susceptible to inhibition by dexamethasone and indomethacin. Furthermore, they suggest that prostaglandins are not involved in the neutrophilia caused by this toxin.

905 Role of Cox-2 enzyme in the interleukin-1-induced slow-wave sleep

1997 ◽  
Vol 28 ◽  
pp. S111
Author(s):  
Akira Terao ◽  
Hitoshi Matsumura ◽  
Shinsuke Satoh ◽  
Masayuki Saito ◽  
Osamu Hayaishi
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Interleukin 1 ◽  
Cox 2

The Effect of Afternoon Body Heating on Body Temperature and Slow Wave Sleep

1990 ◽  
Vol 27 (5) ◽  
pp. 560-566 ◽  
Author(s):  
Jo Jordan ◽  
Iain Montgomery ◽  
John Trinder
Keyword(s):  
Body Temperature ◽  
Slow Wave ◽  
Slow Wave Sleep

Influence of pregnancy on the febrile response to intracerebroventricular administration of PGE1 in rats

1996 ◽  
Vol 81 (3) ◽  
pp. 1312-1315 ◽  
Author(s):  
K. M. Stobie-Hayes ◽  
J. E. Fewell
Keyword(s):  
Prostaglandin E1 ◽  
Interleukin 1 ◽  
Body Core Temperature ◽  
Interleukin 1 Beta ◽  
Cerebral Ventricles ◽  
Endogenous Pyrogen ◽  
Febrile Response ◽  
Pregnant Rats ◽  
Body Core ◽  
Near Term

Rats have an attenuated or absent febrile response to exogenous pyrogen (e.g., bacterial endotoxin) and endogenous pyrogen (e.g., interleukin-1 beta) near term of pregnancy. The present experiments have been carried out on 19 nonpregnant and 18 time-bred pregnant Long-Evans rats to investigate the febrile response to intracerebroventricular (ICV) administration of prostaglandin E1 (PGE1). Each rat was anesthetized, a biotelemetry device was placed in the peritoneal cavity for measurement of body core temperature (Tbc), and guide cannulas were placed above the lateral cerebral ventricles for ICV injection of PGE1. At least 6 days were allowed to lapse between surgery and the experiments. ICV injection of 0.2 micrograms PGE1 produced significant increases in Tbc in both nonpregnant and pregnant animals (day 19 of gestation). The increase in Tbc as well as the fever index, however, were significantly attenuated in the pregnant compared with the nonpregnant rats. Vehicle had no effect on Tbc or fever index in either group of animals. The attenuated febrile response to PGE1 in the pregnant rats may have resulted from a pregnancy-related activation of endogenous antipyretics and/or impaired thermoregulatory effector mechanisms.

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