| Triclosan inhibition of acute and chronic inflammatory gene pathways. | |
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MedLine Citation:
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PMID: 20507366 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM: We sought to determine whether triclosan (2,4,4'-trichloro-2'-hydroxydiphenylether), an extensively used anti-plaque agent with broad-spectrum anti-microbial activity, with reported anti-inflammatory effects via inhibition of prostaglandin E2 and interleukin 1 (IL-1)beta, could also more broadly suppress multiple inflammatory gene pathways responsible for the pathogenesis of gingivitis and periodontitis. MATERIALS AND METHODS: As an exploratory study, the effects of triclosan on the inflammatory gene expression profile were assessed ex vivo using peripheral whole blood samples from eight periodontally healthy donors. Ten-millilitres whole blood aliquots were incubated 2 h with 0.3 microg/ml Escherichia coli lipopolysaccharide (LPS) with or without 0.5 microg/ml triclosan. Affymetrix microarray gene expression profiles from isolated leucocytes and pathway-specific quantitative polymerase chain reaction arrays were used to investigate changes in expression of target cytokines and cell signalling molecules. Results: Ex vivo human whole blood assays indicated that triclosan significantly down-regulated the LPS-stimulated expression of Toll-like receptor signalling molecules and other multiple inflammatory molecules including IL-1 and IL-6 and the dampening of signals that activate the T-helper type 1 acquired immune response via suppression of CD70 with concomitant up-regulation of growth factors related to bone morphogenetic protein (BMP)2 and BMP6 synthesis. Conclusions: Anti-inflammatory effects were found in this exploratory survey, including suppression of microbial-pathogen recognition pathway molecules and the suppression of acute and chronic mediators of inflammation. |
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Authors:
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Silvana P Barros; Sodsi Wirojchanasak; David A Barrow; Fotinos S Panagakos; William Devizio; Steven Offenbacher |
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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: Journal of clinical periodontology Volume: 37 ISSN: 1600-051X ISO Abbreviation: J. Clin. Periodontol. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-05-28 Completed Date: 2010-08-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0425123 Medline TA: J Clin Periodontol Country: Denmark |
Other Details:
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Languages: eng Pagination: 412-8 Citation Subset: D; IM |
Affiliation:
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School of Dentistry, Center for Oral and Systemic Diseases, North Carolina Oral Health Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27709, USA. silvana_barros@dentistry.unc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Adult Anti-Inflammatory Agents / pharmacology* Antigens, CD70 / antagonists & inhibitors Bone Morphogenetic Protein 2 / biosynthesis, genetics Bone Morphogenetic Protein 6 / biosynthesis, genetics Chronic Disease Female Gene Expression Profiling* Host-Pathogen Interactions / drug effects Humans Inflammation / genetics* Inflammation Mediators / antagonists & inhibitors* Interleukin-1 / antagonists & inhibitors, biosynthesis, genetics Interleukin-6 / antagonists & inhibitors, biosynthesis, genetics Lipopolysaccharides / pharmacology Male Oligonucleotide Array Sequence Analysis Signal Transduction / drug effects Th1 Cells / immunology Toll-Like Receptors / antagonists & inhibitors, biosynthesis, genetics* Triclosan / pharmacology* Young Adult |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Antigens, CD70; 0/Bone Morphogenetic Protein 2; 0/Bone Morphogenetic Protein 6; 0/Inflammation Mediators; 0/Interleukin-1; 0/Interleukin-6; 0/Lipopolysaccharides; 0/Toll-Like Receptors; 3380-34-5/Triclosan |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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