Lipopolysaccharide induces visceral hypersensitivity: role of interleukin-1, interleukin-6, and peripheral corticotropin-releasing factor in rats

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.

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Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1 , Interleukin-6, and Tumor Necrosis Factor- in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord

Journal of Neuroscience ◽

10.1523/jneurosci.3338-07.2008 ◽

2008 ◽

Vol 28 (20) ◽

pp. 5189-5194 ◽

Cited By ~ 641

Author(s):

Y. Kawasaki ◽

L. Zhang ◽

J.-K. Cheng ◽

R.-R. Ji

Keyword(s):

Spinal Cord ◽

Tumor Necrosis Factor ◽

Neuronal Activity ◽

Interleukin 6 ◽

Central Sensitization ◽

Tumor Necrosis ◽

Interleukin 1 ◽

Necrosis Factor

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206 Regulation of interleukin-1 and interleukin-6 gene expression in human keratinocytes by ultraviolet radiation: The role of interleukin-1

Journal of Dermatological Science ◽

10.1016/0923-1811(95)93920-v ◽

1995 ◽

Vol 10 (1) ◽

pp. 97

Author(s):

J.H. Chung ◽

S.H. Youn ◽

W.S. Koh ◽

H.C. Eun ◽

K.H. Cho ◽

...

Keyword(s):

Gene Expression ◽

Ultraviolet Radiation ◽

Interleukin 6 ◽

Interleukin 1 ◽

Human Keratinocytes

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Modulation of enteric neurons by interleukin‐6 and corticotropin‐releasing factor contributes to visceral hypersensitivity and altered colonic motility in a rat model of irritable bowel syndrome

The Journal of Physiology ◽

10.1113/jphysiol.2014.279968 ◽

2014 ◽

Vol 592 (23) ◽

pp. 5235-5250 ◽

Cited By ~ 38

Author(s):

Maria M. Buckley ◽

Ken D. O'Halloran ◽

Mark G. Rae ◽

Timothy G. Dinan ◽

Dervla O'Malley

Keyword(s):

Irritable Bowel Syndrome ◽

Rat Model ◽

Interleukin 6 ◽

Colonic Motility ◽

Corticotropin Releasing Factor ◽

Visceral Hypersensitivity ◽

Enteric Neurons ◽

Irritable Bowel

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The effect of interleukin-1 on C-reactive protein expression in Hep3B cells is exerted at the transcriptional level

Biochemical Journal ◽

10.1042/bj3100143 ◽

1995 ◽

Vol 310 (1) ◽

pp. 143-148 ◽

Cited By ~ 55

Author(s):

D Zhang ◽

S L Jiang ◽

D Rzewnicki ◽

D Samols ◽

I Kushner

Keyword(s):

Interleukin 6 ◽

Interleukin 1 ◽

Kinetic Studies ◽

Acute Phase Reactant ◽

Transcriptional Level ◽

Mrna Levels ◽

C Reactive Protein ◽

Reactive Protein ◽

Hep3b Cells

The combination of interleukin 6 (IL-6) and interleukin 1 (IL-1) synergistically induces the human acute-phase reactant, C-reactive protein (CRP) in Hep3B cells. While previous studies have indicated that IL-6 induces transcription of CRP, the mode of action of IL-1 has not been clearly defined. It has been suggested that the effect of IL-1 might be post-transcriptional, exerted through the 5′-untranslated region (5′-UTR). To evaluate the role of IL-1 in CRP gene expression, we studied the effects of interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta) on both the endogenous CRP gene and on transfected CRP-CAT constructs in Hep3B cells. In kinetic studies of the endogenous CRP gene, IL-1 beta alone had no effect on CRP mRNA levels, but when added to IL-6, synergistically enhanced both CRP mRNA levels and transcription, as determined by Northern-blot analyses and nuclear run-on studies. IL-6 alone and the combination of [IL-1 beta + IL-6] each induced increases in mRNA levels roughly comparable with observed increases in transcription. These findings indicate that the effect of IL-1 beta on CRP expression is exerted largely at the transcriptional level in this system. This conclusion was confirmed by studies in Hep3B cells transiently transfected with CRP-CAT constructs, each containing 157 bp of the CRP 5′-flanking region but differing in the length of the 5′-UTR from 104 bp to 3 bp. All constructs responded in the same way; IL-6, but not IL-1 beta, induced significant chloramphenicol acetyltransferase (CAT) expression which was synergistically enhanced 2- to 3-fold by IL-1 beta. These results indicate that IL-1 beta stimulates transcriptional events in the presence of IL-6 and that the upstream 157 bases of the CRP promoter contain elements capable of both IL-6 induction and the synergistic effect of IL-1 beta on transcription.

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