| Delayed activation of PPARgamma by LPS and IFN-gamma attenuates the oxidative burst in macrophages. | |
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MedLine Citation:
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PMID: 11156969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Desensitization of macrophages is important during the development of sepsis. It was our intention to identify mechanisms that promote macrophage deactivation upon contact with endotoxin (LPS) and interferon-gamma (IFN-gamma) in vitro. Macrophage activation was achieved with 12-O-tetradecanoylphorbol 13-acetate (TPA), and the oxidative burst (i.e., oxygen radical formation) was followed by oxidation of the redox-sensitive dyes hydroethidine and dichlorodihydrofluorescein diacetate. Prestimulation of macrophages for 15 h with a combination of LPS/IFN-gamma attenuated oxygen radical formation in response to TPA. Taking the anti-inflammatory properties of the peroxisome proliferator-activating receptorgamma (PPARgamma) into consideration, we established activation of PPARgamma in response to LPS/IFN-gamma by an electrophoretic mobility shift, supershift, and a reporter gene assay. The reporter contains a triple PPAR-responsive element (PPRE) in front of a thymidine kinase minimal promoter driving the luciferase gene. We demonstrated that PPRE decoy oligonucleotides, supplied in front of LPS/IFN-gamma, allowed a full oxidative burst to recover upon TPA addition. Furthermore, we suppressed the oxidative burst by using the PPARgamma agonists 15-deoxy-Delta12,14-prostaglandin J2, BRL 49653, or ciglitazone. No effect was observed with WY 14643, a PPARalpha agonist. We conclude that activation of PPARs, most likely PPARgamma, promotes macrophage desensitization, thus attenuating the oxidative burst. This process appears important during development of sepsis. |
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Authors:
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A Von Knethen A; B Brüne |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: FASEB journal : official publication of the Federation of American Societies for Experimental Biology Volume: 15 ISSN: 0892-6638 ISO Abbreviation: FASEB J. Publication Date: 2001 Feb |
Date Detail:
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Created Date: 2001-02-22 Completed Date: 2001-03-22 Revised Date: 2012-02-15 |
Medline Journal Info:
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Nlm Unique ID: 8804484 Medline TA: FASEB J Country: United States |
Other Details:
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Languages: eng Pagination: 535-44 Citation Subset: IM |
Affiliation:
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Department of Medicine IV-Experimental Division, University of Erlangen-Nürnberg, Faculty of Medicine, 91054 Erlangen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line Cell Survival / drug effects Cells, Cultured Escherichia coli Genes, Reporter Humans Hypoglycemic Agents / pharmacology Interferon-gamma / pharmacology* Lipopolysaccharides / pharmacology* Luciferases / genetics Macrophages / cytology, drug effects, physiology* Mice Microbodies / drug effects, physiology Monocytes / cytology*, drug effects NG-Nitroarginine Methyl Ester / pharmacology Pyrimidines / pharmacology Receptors, Cytoplasmic and Nuclear / agonists, physiology* Recombinant Proteins Respiratory Burst / drug effects, physiology* Tetradecanoylphorbol Acetate / pharmacology Thiazoles / pharmacology Thiazolidinediones* Transcription Factors / agonists, physiology* Transfection |
| Chemical | |
Reg. No./Substance:
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0/Hypoglycemic Agents; 0/Lipopolysaccharides; 0/Pyrimidines; 0/Receptors, Cytoplasmic and Nuclear; 0/Recombinant Proteins; 0/Thiazoles; 0/Thiazolidinediones; 0/Transcription Factors; 122320-73-4/rosiglitazone; 16561-29-8/Tetradecanoylphorbol Acetate; 50892-23-4/pirinixic acid; 50903-99-6/NG-Nitroarginine Methyl Ester; 74772-77-3/ciglitazone; 82115-62-6/Interferon-gamma; EC 1.13.12.-/Luciferases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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