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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
1999-3-25
|
| pubmed:abstractText |
Noradrenaline (NA) and adrenaline (Ad) are modulators of cytokine production. Here we investigated the role of these neurotransmitters in the regulation of macrophage inflammatory protein (MIP)-1alpha expression. Pretreatment of RAW 264.7 macrophages with NA or Ad decreased, in a concentration-dependent manner (1 nM-100 microM), MIP-1alpha release induced by bacterial lipopolysaccharide (LPS 10 ng ml(-1) LPS). The effect of NA was reversed by the selective beta-adrenoceptor antagonist propranolol (10 microM), but not by the alpha-adrenoceptor antagonist phentolamine (10 microM). In the concentration range of 10 nM-10 microM, isoproterenol, a beta-adrenoceptor agonist, but not phenylephrine (a selective alpha1-adrenoceptor agonist) or UK-14304 (a selective alpha2-adrenoceptor agonist) mimicked the inhibitory effects of catecholamines on MIP-1alpha production. Increases in intracellular cyclic adenosine monophosphate, elicited either by the selective type IV phosphodiesterase inhibitor rolipram (0.1 - 10 microM), or by prostaglandin E2, (10 nM-10 microM) decreased MIP-1alpha release, suggesting that increased cyclic AMP may contribute to the suppression of MIP-1alpha release by beta-adrenoceptor stimulation. Northern blot analysis demonstrated that NA (100 nM-10 microM), Ad, isoproterenol, as well as rolipram (100 nM-10 microM) decreased LPS-induced MIP-1alpha mRNA accumulation. NA and Ad (1-100 microM) also decreased MIP-1alpha production in thioglycollate-elicited murine peritoneal macrophages. Pretreatment of mice with either isoproterenol (10 mg kg(-1), i.p.) or rolipram (25 mg kg(-1), i.p.) decreased LPS-induced plasma levels of MIP-1alpha, while propranolol (10 mg kg(-1), i.p.) augmented the production of this chemokine, confirming the role of a beta-adrenoceptor mediated endogenous catecholamine action in the regulation of MIP-1alpha production in vivo. Thus, based on our data we conclude that catecholamines are important endogenous regulators of MIP-1alpha expression in inflammation.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Epinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Thioglycolates
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0007-1188
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
125
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1297-303
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| pubmed:dateRevised |
2008-11-20
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| pubmed:meshHeading |
pubmed-meshheading:9863660-Adrenergic alpha-Agonists,
pubmed-meshheading:9863660-Adrenergic beta-Agonists,
pubmed-meshheading:9863660-Animals,
pubmed-meshheading:9863660-Antibody Formation,
pubmed-meshheading:9863660-Cell Adhesion,
pubmed-meshheading:9863660-Cells, Cultured,
pubmed-meshheading:9863660-Chemokine CCL3,
pubmed-meshheading:9863660-Chemokine CCL4,
pubmed-meshheading:9863660-Cyclic AMP,
pubmed-meshheading:9863660-Epinephrine,
pubmed-meshheading:9863660-Isoproterenol,
pubmed-meshheading:9863660-Lipopolysaccharides,
pubmed-meshheading:9863660-Macrophage Inflammatory Proteins,
pubmed-meshheading:9863660-Macrophages, Peritoneal,
pubmed-meshheading:9863660-Male,
pubmed-meshheading:9863660-Mice,
pubmed-meshheading:9863660-Mice, Inbred BALB C,
pubmed-meshheading:9863660-Norepinephrine,
pubmed-meshheading:9863660-RNA, Messenger,
pubmed-meshheading:9863660-Receptors, Adrenergic, beta,
pubmed-meshheading:9863660-Sympathetic Nervous System,
pubmed-meshheading:9863660-Thioglycolates
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| pubmed:year |
1998
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| pubmed:articleTitle |
Exogenous and endogenous catecholamines inhibit the production of macrophage inflammatory protein (MIP) 1 alpha via a beta adrenoceptor mediated mechanism.
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| pubmed:affiliation |
Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
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| pubmed:publicationType |
Journal Article
|