Toll-like receptor expression on peripheral blood mononuclear cells in asthmatics; implications for asthma management
E Chun, SH Lee, SY Lee, EJ Shim, SH Cho… - Journal of Clinical …, 2010 - Springer
Journal of Clinical Immunology, 2010•Springer
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-α, IL-1β, IL-6, IL-8, and IFN-
γ) on the peripheral blood mononuclear cells (PBMCs) of 36 stable asthmatics on treatment …
(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-α, IL-1β, IL-6, IL-8, and IFN-
γ) on the peripheral blood mononuclear cells (PBMCs) of 36 stable asthmatics on treatment …
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-α, IL-1β, IL-6, IL-8, and IFN-γ) on the peripheral blood mononuclear cells (PBMCs) of 36 stable asthmatics on treatment (the on-treatment group), 15 asthmatics (the treatment-naïve 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-α production stimulated by lipopolysaccharide (LPS), were significantly higher in mild to moderate than in severe asthmatics. Interestingly, in the treatment-naïve group, short-term prednisolone significantly increased LPS-induced TNF-α and IFN-γ 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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