Abstract
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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Abbreviations
- LPS:
-
Lipopolysaccharide
- PAMPs:
-
Pathogen-associated molecular patterns
- PBMCs:
-
Peripheral blood mononuclear cells
- PGN:
-
Peptidoglycan
- TLRs:
-
Toll-like receptors
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Acknowledgments
This work was supported by a grant of the Korea Health 21 R&D Project (A030001) from the Ministry of Health and Welfare, Republic of Korea, and by a grant from Seoul National University Hospital (0420061070).
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Chun, E., Lee, SH., Lee, SY. et al. Toll-like Receptor Expression on Peripheral Blood Mononuclear Cells in Asthmatics; Implications for Asthma Management. J Clin Immunol 30, 459–464 (2010). https://doi.org/10.1007/s10875-009-9363-z
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DOI: https://doi.org/10.1007/s10875-009-9363-z