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Toll-like receptor expression on peripheral blood mononuclear cells in asthmatics; implications for asthma management.

Authors: Chun, E  Lee, SH  Lee, SY  Shim, EJ  Cho, SH  Min, KU  Kim, YY  Park, HW 
Citation: Chun E, etal., J Clin Immunol. 2010 May;30(3):459-64. Epub 2010 Jan 14.
Pubmed: (View Article at PubMed) PMID:20072849
DOI: Full-text: DOI:10.1007/s10875-009-9363-z

BACKGROUND: Accumulating evidence indicates that cells expressing Toll-like receptors (TLRs) play an important role in allergic diseases. The authors undertook this study to explore the hypothesis that TLR-mediated inflammatory signals are important from the perspective of asthma management. METHODS: The expressions of TLR1, TLR2, TLR3, TLR4, TLR6, and TLR9 and levels of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-8, and IFN-gamma) on the peripheral blood mononuclear cells (PBMCs) of 36 stable asthmatics on treatment (the on-treatment group), 15 asthmatics (the treatment-naive group) before and after a 7-day course of oral prednisolone (30 mg/day), and on the PBMCs of 15 healthy controls were measured after in vitro stimulation using TLR-specific ligands. RESULTS: In the on-treatment group, TLR1, TLR2, TLR6, and TLR9 expressions on PBMCs were significantly different between asthmatics and controls. And the expression of TLR4 on PBMCs and TNF-alpha production stimulated by lipopolysaccharide (LPS), were significantly higher in mild to moderate than in severe asthmatics. Interestingly, in the treatment-naive group, short-term prednisolone significantly increased LPS-induced TNF-alpha and IFN-gamma productions by PBMCs. CONCLUSION: TLR-mediated inflammatory signals contribute to the development and severity of asthma and are not reduced by glucocorticoid treatment, which suggests that a TLR-specific antagonist and glucocorticoid are required for the effective control of airway inflammation in asthmatics.


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CRRD Object Information
CRRD ID: 4889523
Created: 2010-12-03
Species: All species
Last Modified: 2010-12-03
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.