Effect of three composite recipes on content of monoamine transmitters in hypothalamus induced by intracerebroventricular injection of interleukin-1 in rats

1999 ◽  
Vol 5 (2) ◽  
pp. 130-130
Author(s):  
Duan Yuanli ◽  
Zhang Xinmin ◽  
Shen Ziyin ◽  
Wang Wenjian ◽  
Chen Weihua
Keyword(s):  
Interleukin 1 ◽  
Intracerebroventricular Injection ◽  
Monoamine Transmitters

Suppression of splenic macrophage interleukin-1 secretion following intracerebroventricular injection of interleukin-1β: Evidence for pituitary-adrenal and sympathetic control

1991 ◽  
Vol 132 (1) ◽  
pp. 84-93 ◽  
Author(s):  
Richard Brown ◽  
Zuo Li ◽  
Catherine Y. Vriend ◽  
Raminder Nirula ◽  
Loren Janz ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Interleukin 1Β ◽  
Intracerebroventricular Injection ◽  
Splenic Macrophage ◽  
Sympathetic Control

Increased Circulating Interleukin-1 and Interleukin-6 after Intracerebroventricular Injection of Lipopolysaccharide

1992 ◽  
Vol 56 (6) ◽  
pp. 935-938 ◽  
Author(s):  
Paul E. Gottschall ◽  
Gen Komaki ◽  
Akira Arimura
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1 ◽  
Intracerebroventricular Injection

Intracerebroventricular Injection of Interleukin-1 Suppresses Peripheral Lymphocyte Function in the Primate

1997 ◽  
Vol 4 (1) ◽  
pp. 12-18 ◽  
Author(s):  
G.M. Sullivan ◽  
S.M. Canfield ◽  
S. Lederman ◽  
E. Xiao ◽  
M. Ferin ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Peripheral Lymphocyte ◽  
Lymphocyte Function ◽  
Intracerebroventricular Injection

Lipocortin 1 fragment modifies pyrogenic actions of cytokines in rats

1990 ◽  
Vol 259 (2) ◽  
pp. R266-R269 ◽  
Author(s):  
F. Carey ◽  
R. Forder ◽  
M. D. Edge ◽  
A. R. Greene ◽  
M. A. Horan ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Interleukin 1 ◽  
Physiological Role ◽  
Polyclonal Antiserum ◽  
Intracerebroventricular Injection ◽  
Interleukin 1 Beta ◽  
Recombinant Fragment ◽  
Central Effects ◽  
Colonic Temperature ◽  
Dose Dependent

Lipocortins form a group of proteins that have been proposed as mediators of the anti-inflammatory actions of glucocorticoids. Intracerebroventricular injection of a recombinant fragment of lipocortin 1 (NH2-terminal 1-188) caused dose-dependent (0.4-1.2 micrograms) reductions in the acute increases in colonic temperature and oxygen consumption, which occurred in response to central injections of recombinant interleukin 1 beta and gamma-interferon in conscious rats. In contrast the lipocortin fragment did not affect the response to prostaglandin E2, and its activity was prevented by heat treatment or by pretreatment of animals with polyclonal antiserum raised to the fragment. Central injection of antiserum significantly enhanced the thermogenic responses to interleukin 1 beta in rats treated with dexamethasone without affecting the responses in normal animals. These results support a physiological role for lipocortin in the central effects of glucocorticoids.

Interleukin-1 induces changes in sleep, brain temperature, and serotonergic metabolism

1997 ◽  
Vol 272 (2) ◽  
pp. R601-R606 ◽  
Author(s):  
C. Gemma ◽  
L. Imeri ◽  
M. G. de Simoni ◽  
M. Mancia
Keyword(s):  
Time Course ◽  
Preoptic Area ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Secondary Effect ◽  
Intracerebroventricular Injection ◽  
Early Increase ◽  
Cortical Temperature ◽  
Freely Moving

Simultaneous recordings of sleep-wake activity and of serotonergic metabolism in the medial preoptic area were performed in freely moving rats after the intracerebroventricular injection of interleukin-1 (IL-1) at dark onset. IL-1 (2.5 ng) induced a biphasic increase in slow-wave sleep and an early increase in serotonergic metabolism starting 30 min postinjection. Phasic, state-specific changes (which have been described in spontaneous sleep) were superimposed on this tonic, overall increase in serotonergic metabolism. IL-1 (25 ng) induced an increase in wakefulness and a delayed increase in serotonergic metabolism, which started 120 min postinjection. This suggests that the time course of the serotonergic activation could play a role in mediating IL-1 effects on sleep. Both doses of IL-1 induced a similar and significant increase in brain cortical temperature, suggesting that IL-1 effects on sleep are not a secondary effect of the increase in cortical temperature and that the serotonergic system is not involved in IL-1-induced fever.

Importance of brain IL-1 type II receptors in fever and thermogenesis in the rat

1993 ◽  
Vol 265 (4) ◽  
pp. E585-E591 ◽  
Author(s):  
G. Luheshi ◽  
S. J. Hopkins ◽  
R. A. Lefeuvre ◽  
M. J. Dascombe ◽  
P. Ghiara ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Low Dose ◽  
Interleukin 1 ◽  
Type I ◽  
Intracerebroventricular Injection ◽  
Type Ii ◽  
Central Effects ◽  
Conscious Rats ◽  
Central Actions ◽  
The Brain

Interleukin-1 (IL-1) acts centrally to induce fever and thermogenesis in rodents. The central actions of IL-1 alpha and IL-1 beta apparently involve different mechanisms, and the effects of IL-1 beta are not consistent with interaction with a type I (IL-1RI) 80-kDa receptor. In the present study the involvement of the type II IL-1 receptor (IL-1RII) was tested in the rat by examining the effects of central injection of a monoclonal antibody (ALVA-42), which blocks the IL-1RII. Pretreatment of rats with ALVA-42 (6 micrograms icv) inhibited the thermogenic and pyrogenic responses to intracerebroventricular injection of 5 ng (but not 50 ng) of IL-1 beta in conscious rats but did not significantly modify responses to IL-1 alpha. ALVA-42 also failed to modify the responses to peripherally administered IL-1 beta (1 microgram) but significantly attenuated the pyrogenic and thermogenic responses to peripheral (125 micrograms) or central (1 microgram) injection of endotoxin. These data indicate that IL-1RII mediates the central effects of a low dose of IL-1 beta, but not IL-1 alpha, on fever and thermogenesis in the rat. They also imply that responses to endotoxin are due, at least in part, to the activation of IL-1RII by IL-1 beta released within the brain and that effects of peripherally injected IL-1 beta involve different mechanisms, probably associated with IL-1RI.

Characteristics of fever and acute-phase response induced in rabbits by IL-1 and TNF

1989 ◽  
Vol 256 (1) ◽  
pp. R35-R41 ◽  
Author(s):  
A. Morimoto ◽  
Y. Sakata ◽  
T. Watanabe ◽  
N. Murakami
Keyword(s):  
Plasma Concentration ◽  
Intravenous Injection ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Leukocyte Count ◽  
Interleukin 1 ◽  
Phase Response ◽  
Peripheral Target ◽  
Intracerebroventricular Injection ◽  
Target Organs

We investigated the effect of human recombinant interleukin 1 alpha (hrIL-1 alpha) and human recombinant tumor necrosis factor (hrTNF) on body temperature and acute-phase response, including changes in the plasma concentration of iron, zinc, and copper and in circulating leukocyte count. The intravenous injection of a smaller dose of either hrIL-1 alpha (0.5 micrograms/kg) or hrTNF (2 micrograms/kg) produced a monophasic fever, whereas a larger dose (hrIL-1 alpha, 2 micrograms/kg; hrTNF, 10 micrograms/kg) produced a biphasic fever. The intracerebroventricular injection of hrIL-1 alpha or hrTNF produced a dose-dependent fever. The intravenous injection of either hrIL-1 alpha or hrTNF decreased the plasma concentration of iron and zinc and increased the plasma copper concentration and the circulating leukocyte count. The intracerebroventricular injection of hrIL-1 alpha induced those responses, although the intracerebroventricular injection of hrTNF did not. The present results show that two kinds of monokines, hrIL-1 alpha and hrTNF, are intrinsically pyrogenic and induce the acute-phase response. Furthermore, it is suggested that hrIL-1 alpha induces febrile and acute-phase responses through its action on both the peripheral target organs and the central nervous system. However, hrTNF induces those responses only by its action on the peripheral target organs outside the blood-brain barrier.

scholarly journals Interleukin-1 Mediates the Anorexic and Febrile Actions of Galanin-Like Peptide

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5791-5802 ◽  
Author(s):  
Pui-Sin Man ◽  
Catherine B. Lawrence
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Interleukin 1 ◽  
Brain Regions ◽  
Type I ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Rats And Mice

Galanin-like peptide (GALP) is a neuropeptide that has complex actions on energy balance, producing orexigenic effects in the short term in rats but anorexigenic and febrile effects over the longer term in rats and mice. GALP is thought to promote feeding via neuropeptide Y and orexin neurons, but the mediators of the anorexia are unknown. However, the anorexic and febrile actions of GALP are similar in magnitude and profile to those seen after central injections of the cytokine IL-1. Thus, the aim of this study was to test the hypothesis that IL-1 mediates the effects of GALP on energy balance. Intracerebroventricular injection of GALP (1.5 nmol) in male Sprague-Dawley rats stimulated production of IL-1α and IL-1β protein in macrophages and/or microglia in selected brain areas, including the meninges, and periventricular brain regions. Intracerebroventricular injection of GALP in rats stimulated food intake over 1 h but decreased feeding and body weight at 24 h and caused a rise in core body temperature over 8 h. Coinfusion of the IL-1 receptor antagonist had no effect on the GALP-induced orexigenic response but significantly reduced the longer-term actions of GALP observed at 24 h and its effect on body temperature. Furthermore, the actions of GALP on feeding, body weight, and body temperature were significantly reduced in IL-1α/β-, IL-1β-, or IL-1 type I receptor (IL-1RI)-deficient mice. These data suggest that GALP induces expression of IL-1 in the brain, and its anorexic and febrile actions are mediated by this cytokine acting via IL-1 type I receptor.

Interleukin-1 receptor antagonist inhibits endotoxin fever and systemic interleukin-6 induction in the rat

1996 ◽  
Vol 270 (1) ◽  
pp. E91-E95 ◽  
Author(s):  
G. Luheshi ◽  
A. J. Miller ◽  
S. Brouwer ◽  
M. J. Dascombe ◽  
N. J. Rothwell ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Receptor Antagonist ◽  
Interleukin 6 ◽  
Single Injection ◽  
Interleukin 1 ◽  
Intracerebroventricular Injection ◽  
Febrile Response ◽  
Interleukin 1 Receptor Antagonist ◽  
The Brain ◽  
Pyrogenic Activity

Although a number of studies indicate that the pyrogenic activity of lipopolysaccharide (LPS) and/or interleukin (IL)-1 is mediated via induction of IL-6, this has been questioned by recent evidence demonstrating a dissociation between fever and circulating IL-6. The present study reexamines this relationship by use of human recombinant interleukin-1 receptor antagonist (IL-1ra). Injection of LPS (100 micrograms/kg ip) into rats induced fever (2.0 degrees C) that was significantly inhibited (P < 0.05) when IL-1ra (16 mg/kg ip) was given 1 and 2 h after LPS. The rise in plasma IL-6 preceded the febrile response by 1-1.5 h and, although the concentrations of bioactive IL-6 in plasma and cerebrospinal fluid (CSF) were not reduced at 4 h, at 2 h plasma and CSF IL-6 bioactivity was inhibited by 80 and 70%, respectively, after a single injection of IL-1ra (16 mg/kg ip). Intracerebroventricular injection of IL-1ra (200 micrograms/rat) inhibited LPS fever but did not affect the plasma IL-6 bioactivity measured 2 or 4 h after intraperitoneal LPS. These data show that peripheral IL-1 plays a part in the induction of both fever and the rise in plasma IL-6 that precedes it, and that IL-1 within the brain is also important in the induction of fever by LPS.

Sign in / Sign up

Export Citation Format

Share Document