Cited 21 times since 2004 (1.1 per year) source: EuropePMC The Journal of allergy and clinical immunology, Volume 114, Issue 4, 1 1 2004, Pages 791-798 TGF-beta differentially regulates TH2 cytokine-induced eotaxin and eotaxin-3 release by human airway smooth muscle cells. Zuyderduyn S, Hiemstra PS, Rabe KF
Background
Human airway smooth muscle cells (HASMs) are involved in the pathogenesis of asthma. By producing chemokines, HASMs play a role in the inflammatory processes observed in this disease. Eotaxin, eotaxin-2, and eotaxin-3 are important chemoattractants for eosinophils, and these chemokines are expressed during different phases of the allergic reaction. TH2 cytokines and TGF-beta can be found in increased levels in patients with asthma, and these cytokines may be involved in the regulation of chemokine expression.
Objective
The aim of this study was to determine the effect of TH2 cytokines and TGF-beta on the regulation of expression of eotaxin, eotaxin-2, and eotaxin-3 by HASMs.
Methods
HASMs were incubated for 24 hours with IL-4, IL-13, TGF-beta1, or combinations of these cytokines. Protein and mRNA levels of eotaxin and eotaxin-3 were evaluated by sandwich ELISA and reverse transcriptase-PCR.
Results
IL-4 and IL-13 induced mRNA and protein for both eotaxin and eotaxin-3. Eotaxin-2 mRNA and protein were not detected in HASMs. TGF-beta alone did not induce expression of the eotaxins. However, in combination with IL-4 or IL-13, TGF-beta enhanced eotaxin production and inhibited TH2 cytokine-induced eotaxin-3 production.
Conclusion
TGF-beta differentially regulates TH2 cytokine-induced eotaxin and eotaxin-3 release.
