Document Detail


Staphylococcus aureus membrane and diacylated lipopeptide induce thymic stromal lymphopoietin in keratinocytes through the Toll-like receptor 2-Toll-like receptor 6 pathway.
MedLine Citation:
PMID:  21050945     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Staphylococcus aureus heavily colonizes the lesions of patients with atopic dermatitis (AD) and is known to trigger a worsening of AD. However, the exact mechanism by which S. aureus promotes AD is unknown. Thymic stromal lymphopoietin (TSLP), which is highly expressed by keratinocytes in skin lesions of patients with AD and bronchial epithelial cells in asthmatic patients, represents a critical factor linking responses at interfaces between the body and the environment to allergic type 2 immune responses.
OBJECTIVES: We sought to examine the ability of synthetic lipopeptides and S. aureus to induce TSLP expression in human keratinocytes and identify the pathway of induction.
METHODS: We stimulated primary human keratinocytes with lipopeptides and S. aureus-derived materials. The release and gene expression of TSLP were measured by means of ELISA and quantitative PCR, respectively.
RESULTS: Diacylated lipopeptide upregulated the expression of TSLP and other proinflammatory molecules. Heat-killed S. aureus and the subcellular fractions of S. aureus induced TSLP's release, with the membranous fraction having the greatest activity. Small interfering RNA-mediated knockdown of either Toll-like receptor (TLR) 2 or TLR6 inhibited the diacylated lipopeptide- and S. aureus membrane-induced TSLP gene expression. S. aureus membrane- and diacylated lipopeptide-induced release of TSLP was enhanced by T(H)2/TNF-α cytokines and partially suppressed by IFN-γ and TGF-β.
CONCLUSIONS: The results suggest that ligands for the TLR2-TLR6 heterodimer in S. aureus membranes, including diacylated lipoproteins, could promote T(H)2-type inflammation through TSLP production in keratinocytes, providing an overall picture of the vicious cycles between colonization by S. aureus and AD in the T(H)2-skewed sensitization process, exacerbation of the disease, or both.
Authors:
Anh Tuan Vu; Tadashi Baba; Xue Chen; Tuan Anh Le; Hirokazu Kinoshita; Yang Xie; Seiji Kamijo; Keiichi Hiramatsu; Shigaku Ikeda; Hideoki Ogawa; Ko Okumura; Toshiro Takai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  126     ISSN:  1097-6825     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-05     Completed Date:  2010-12-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  985-93, 993.e1-3     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
Affiliation:
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
Antigens, Bacterial / immunology*
Cell Membrane / immunology
Cytokines / biosynthesis,  immunology*
Dermatitis, Atopic / immunology,  metabolism,  microbiology*
Enzyme-Linked Immunosorbent Assay
Gene Expression
Humans
Keratinocytes / immunology*,  secretion
Lipopeptides / immunology
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / immunology
Staphylococcal Infections / immunology
Staphylococcus aureus / immunology
Toll-Like Receptor 2 / immunology*
Toll-Like Receptor 6 / immunology*
Chemical
Reg. No./Substance:
0/Antigens, Bacterial; 0/Cytokines; 0/Lipopeptides; 0/TLR2 protein, human; 0/TLR6 protein, human; 0/Toll-Like Receptor 2; 0/Toll-Like Receptor 6; 0/thymic stromal lymphopoietin

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