| Sequential expression of macrophage anti-microbial/inflammatory and wound healing markers following innate, alternative and classical activation. | |
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MedLine Citation:
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PMID: 20059482 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The present study examines the temporal dynamics of macrophage activation marker expression in response to variations in stimulation. We demonstrate that markers can be categorized as 'early' (expressed most abundantly at 6 h post-stimulation) or 'late' (expressed at 24 h post-stimulation). Thus nos2 and p40 (IL-12/IL-23) are early markers of innate and classical activation, while dectin-1 and mrc-1 are early markers and fizz1 (found in inflammatory zone-1) and ym1 are late markers of alternative activation. Furthermore, argI is a late marker of both innate and alternative activation. The ability of interferon (IFN)-gamma to alter these activation markers was studied at both the protein level and gene level. As reported previously, IFN-gamma was able to drive macrophages towards the classical phenotype by enhancing nos2 gene expression and enzyme activity and p40 (IL-12/IL-23) gene expression in lipopolysaccharide (LPS)-stimulated macrophages. IFN-gamma antagonized alternative macrophage activation, as evident by reduced expression of dectin-1, mrc-1, fizz1 and ym1 mRNA transcripts. In addition, IFN-gamma antagonized arginase activity irrespective of whether macrophages were activated innately or alternatively. Our data explain some apparent contradictions in the literature, demonstrate temporal plasticity in macrophage activation states and define for the first time 'early' and 'late' markers associated with anti-microbial/inflammatory and wound healing responses, respectively. |
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Authors:
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F M Menzies; F L Henriquez; J Alexander; C W Roberts |
Publication Detail:
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Type: Journal Article Date: 2010-01-05 |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 160 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-06-18 Completed Date: 2010-07-09 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 369-79 Citation Subset: IM |
Affiliation:
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Strathclyde Institute for Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antiviral Agents / pharmacology Arginase / biosynthesis, immunology Biological Markers / metabolism Gene Expression Regulation / drug effects, immunology* Immunity, Innate / drug effects, immunology Inflammation Mediators / immunology*, metabolism Intercellular Signaling Peptides and Proteins / biosynthesis, immunology Interferon-gamma / pharmacology Interleukin-12 Subunit p40 / biosynthesis, immunology Lectins / biosynthesis, immunology Macrophage Activation / drug effects, immunology* Macrophages / immunology*, metabolism Male Membrane Proteins / biosynthesis, immunology Mice Mice, Inbred BALB C Nerve Tissue Proteins / biosynthesis, immunology Nitric Oxide Synthase Type II / biosynthesis, immunology Wound Healing / drug effects, immunology* beta-N-Acetylhexosaminidases / biosynthesis, immunology |
| Chemical | |
Reg. No./Substance:
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0/Antiviral Agents; 0/Biological Markers; 0/Inflammation Mediators; 0/Intercellular Signaling Peptides and Proteins; 0/Interleukin-12 Subunit p40; 0/Lectins; 0/Membrane Proteins; 0/Nerve Tissue Proteins; 0/Retnla protein, mouse; 0/dectin 1; 82115-62-6/Interferon-gamma; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse; EC 3.2.1.52/Chi3l3 protein, mouse; EC 3.2.1.52/beta-N-Acetylhexosaminidases; EC 3.5.3.1/Arg1 protein, mouse; EC 3.5.3.1/Arginase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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