Febrile response to tissue inflammation involves both peripheral and brain IL-1 and TNF-alpha in the rat

Luheshi, Giamal N.; Stefferl, Andreas; Turnbull, Andrew V.; Dascombe, Michael J.; Brouwer, S.; Hopkins, Stephen; Rothwell, N. J.

doi:10.1152/ajpregu.1997.272.3.r862

Cited by 60 publications

(75 citation statements)

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“…The difference in the time profiles between IL-6 and TNF-␣ does not preclude the latter from involvement in mediating the fever response to poly I:C, especially since IL-1ra failed to completely abolish the increase in body temperature. We have previously demonstrated that TNF-␣ is involved in mediating fever after localized inflammation in rats (31), and others have shown that it induces COX-2 in the brain (8). The role of TNF in fever, however, remains controversial, with some suggesting that it acts as an endogenous cryogen (26).…”

Section: Discussionmentioning

confidence: 99%

The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism

Fortier

Kent²,

Ashdown³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

278

210

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Section: Discussionmentioning

confidence: 99%

The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism

Fortier

Kent²,

Ashdown³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

278

210

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“…36 In order to determine the source of IL-6 under the experimental conditions, Northern blot analysis of total RNA prepared from skeletal muscle, liver, lung, heart, kidney, spleen, small and large intestine, at various time points after injection of TO, was performed. Total cellular RNA (10 mg) isolated from rat Kupffer cells treated with LPS (500 ng/ml) was processed in parallel and served as a positive control for IL-6-specific transcripts.…”

Section: Induction Of Heme Oxygenase-1 During Inflammation K Tron Et Almentioning

confidence: 99%

“…In this regard, the TO-induced model of the APR is of particular interest because it is accompanied by an increase of circulating IL-6 levels, whereas plasma IL-1b and TNF-a levels remain undetectable. 36 …”

Section: Regulation Of Ho-1 Expression In To Model Of the Apr In Ratsmentioning

confidence: 99%

“…An increased secretion of IL-6 into the bloodstream in TO model has been reported before. 36 Furthermore, it has also been shown that IL-6-deficient mice were unable to maintain a normal inflammatory response to localized tissue damage generated by TO injection. 41 In agreement with these findings, we have demonstrated that serum IL-6 concentrations were markedly elevated after TO injection (Figure 4).…”

Section: Expression Of Il-6 After To Administration and Its Possible mentioning

confidence: 99%

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Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6

Tron¹,

Novosyadlyy²,

Dudás³

et al. 2005

Laboratory Investigation

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Heme oxygenase-1 (HO-1) is the inducible isoform of an enzyme family responsible for heme degradation and was suggested to be involved in the acute phase response in the liver. However, the mechanisms of the HO-1 regulation under inflammatory conditions are poorly understood. Therefore, the purpose of the current work was to study the expression of HO-1 in the liver and other organs of rats with a localized inflammation after intramuscular injection of turpentine oil (TO). Since interleukin-6 (IL-6) is known to be a principal mediator of inflammation, the levels of this cytokine were also estimated in the animal model used. HO-1 and IL-6 expression was evaluated by Northern blot, in situ hybridization, Western blot, immunohistochemistry and enzyme-linked immunosorbent assay. In the liver and injured muscle, the HO-1 mRNA levels were dramatically increased 4-6 h after TO administration. HO-1 protein levels in the liver were elevated starting from 6-12 h after the treatment. In other internal organs such as the heart, kidney and large intestine, only a slight induction of HO-1 mRNA was observed. IL-6-specific transcripts appeared only in the injured muscle and were in accordance with serum levels of IL-6. In turn, temporal expression of IL-6 in the muscle and circulatory IL-6 levels correlated well with HO-1 expression in the liver and injured muscle. In the liver of control rats HO-1 protein was detected in Kupffer cells, while in TO-injected rats also hepatocytes became strongly HO-1 positive. Conversely, in the injured muscle, HO-1 immunoreactivity was attributed only to macrophages. Our data demonstrate that during localized inflammation HO-1 expression was rapidly and strongly induced in macrophages of injured muscle and in hepatocytes, and IL-6 derived from injured muscle seems to be responsible for the HO-1 induction in the liver.

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“…IL-1 mediates several of the physiological and behavioral changes in response to a systemic inflammatory challenge induced by the bacterial endotoxin, lipopolysaccharide (LPS), or turpentine (Long et al, 1990;Luheshi et al, 1996Luheshi et al, , 1997Miller et al, 1997b). IL-1 may act by inducing the expression of an array of downstream mediators, several of which are pertinent to the systemic inflammatory response after stroke, in particular IL-6 and che-mokines (Miller et al, 1997b;Cartmell et al, 2000;Calkins et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Systemic Inflammatory Stimulus Potentiates the Acute Phase and CXC Chemokine Responses to Experimental Stroke and Exacerbates Brain Damage via Interleukin-1- and Neutrophil-Dependent Mechanisms

McColl¹,

Rothwell

Allan³

2007

J. Neurosci.

Self Cite

314

338

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Systemic inflammatory stimuli, such as infection, increase the risk of stroke and are associated with poorer clinical outcome. The mechanisms underlying the impact of systemic inflammatory stimuli on stroke are not well defined. We investigated the impact of systemic inflammation on experimental stroke and potential mechanisms involved. Focal cerebral ischemia was induced by intraluminal filament occlusion of the middle cerebral artery (MCAo). Brain damage and neurological deficit 24 h after MCAo were exacerbated by systemic lipopolysaccharide (LPS) administration. This exacerbation was critically dependent on interleukin (IL)-1, because coadministration of IL-1 receptor antagonist abolished the effect of LPS on brain damage. Systemic administration of IL-1 increased ischemic damage to a similar extent as LPS and also exacerbated brain edema. IL-1 markedly potentiated circulating levels of the acute phase proteins, serum amyloid A and IL-6, and the neutrophil-selective CXC chemokines, KC and macrophage inflammatory protein-2. Neutrophil mobilization and cortical neutrophil infiltration were aggravated by IL-1 before changes in ischemic damage. Neutropenia abolished the damaging effects of systemic IL-1. These data show for the first time that an acute systemic inflammatory stimulus is detrimental to outcome after experimental stroke and highlight IL-1 as a critical mediator in this paradigm. Our data suggest IL-1-induced potentiation of neutrophil mobilization via CXC chemokine induction is a putative mechanism underlying this effect. Our results may help to explain the poorer outcome in stroke patients presenting with infection and may have implications for neurodegenerative diseases involving neurovascular alterations, such as Alzheimer's disease, in which systemic inflammation can modulate disease progression.

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Febrile response to tissue inflammation involves both peripheral and brain IL-1 and TNF-alpha in the rat

Cited by 60 publications

References 0 publications

The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism

The viral mimic, polyinosinic:polycytidylic acid, induces fever in rats via an interleukin-1-dependent mechanism

Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6

Systemic Inflammatory Stimulus Potentiates the Acute Phase and CXC Chemokine Responses to Experimental Stroke and Exacerbates Brain Damage via Interleukin-1- and Neutrophil-Dependent Mechanisms

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