| Effect of the antimicrobial peptide LL-37 on Toll-like receptors 2-, 3- and 4-triggered expression of IL-6, IL-8 and CXCL10 in human gingival fibroblasts. | |
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MedLine Citation:
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PMID: 20570250 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The antimicrobial peptide LL-37 is known to have a potent LPS-neutralizing activity in monocytes and macrophages. Recently, LL-37 in gingival crevicular fluids is suggested to be the major protective factor preventing infection of periodontogenic pathogens. In this study, we tried to address the effect of LL-37 on proinflammatory responses of human gingival fibroblasts (HGFs) stimulated with Toll-like receptor (TLR)-stimulant microbial compounds. LL-37 potently suppressed LPS-induced gene expression of IL6, IL8 and CXCL10 and intracellular signaling events, degradation of IRAK-1 and IkappaBalpha and phosphorylation of p38 MAPK and IRF3, indicating that the LPS-neutralizing activity is also exerted in HGFs. LL-37 also suppressed the expression of IL6, IL8 and CXCL10 induced by the TLR3 ligand poly(I:C). LL-37 modestly attenuated the expression of IL6 and IL8 induced by the TLR2/TLR1 ligand Pam(3)CSK(4), but did not affect the expression induced by the TLR2/TLR6 ligand MALP-2. Interestingly, LL-37 rather upregulated the expression of IL6, IL8 and CXCL10 induced by another TLR2/TLR6 ligand FSL-1. Thus, the regulatory effect of LL-37 is differently exerted towards proinflammatory responses of HGFs induced by different microbial stimuli, which may lead to unbalanced proinflammatory responses of the gingival tissue to infection of oral microbes. |
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Authors:
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T Into; M Inomata; K Shibata; Y Murakami |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-15 |
Journal Detail:
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Title: Cellular immunology Volume: 264 ISSN: 1090-2163 ISO Abbreviation: Cell. Immunol. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-07-12 Completed Date: 2010-09-01 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1246405 Medline TA: Cell Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 104-9 Citation Subset: IM |
Copyright Information:
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2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Oral Microbiology, Asahi University School of Dentistry, 1851-1 Hozumi, Mizuho, Gifu 501-0296, Japan. into@dent.asahi-u.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antimicrobial Cationic Peptides
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pharmacology* Bacterial Infections / immunology Cells, Cultured Chemokine CXCL10 / biosynthesis*, genetics, secretion Fibroblasts / drug effects*, immunology, metabolism, pathology Gene Expression Regulation Gingiva / pathology Humans Immunity, Innate Interleukin-1 Receptor-Associated Kinases / antagonists & inhibitors Interleukin-6 / biosynthesis*, genetics, secretion Interleukin-8 / biosynthesis*, genetics, secretion Ligands Periodontal Diseases / immunology Signal Transduction / drug effects Toll-Like Receptor 2 / immunology, metabolism Toll-Like Receptor 3 / immunology, metabolism Toll-Like Receptor 4 / immunology, metabolism p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors |
| Chemical | |
Reg. No./Substance:
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0/Antimicrobial Cationic Peptides; 0/Chemokine CXCL10; 0/Interleukin-6; 0/Interleukin-8; 0/Ligands; 0/TLR2 protein, human; 0/TLR3 protein, human; 0/TLR4 protein, human; 0/Toll-Like Receptor 2; 0/Toll-Like Receptor 3; 0/Toll-Like Receptor 4; 143108-26-3/CAP18 lipopolysaccharide-binding protein; EC 2.7.11.1/Interleukin-1 Receptor-Associated Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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