TGF-β differentially regulates TH2 cytokine-induced eotaxin and eotaxin-3 release by human airway smooth muscle cells

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY

卷:114

Article

Zuyderduyn, S ; Hiemstra, PS ; Rabe, KF

关键词: human airway smooth muscle cells;    T(H)2 cytokines;    TGF-beta;    chemokines;    allergy;    asthma;   

DOI  :  10.1016/j.jaci.2004.06.037

来源: Elsevier

【 摘 要 】

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. T(H)2 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 T(H)2 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 T(H)2 cytokine-induced eotaxin-3 production. Conclusion: TGF-beta differentially regulates T(H)2 cytokine-induced eotaxin and eotaxin-3 release.

【 授权许可】

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