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Am. J. Respir. Cell Mol. Biol., Volume 19, Number 3, September, 1998 400-407

beta -Adrenoceptor-mediated Inhibition of IFN-gamma , IL-3, and GM-CSF mRNA Accumulation in Activated Human T Lymphocytes Is Solely Mediated by the beta 2-Adrenoceptor Subtype

Peter Borger, Yke Hoekstra, Mariet T. Esselink, Dirkje S. Postma, Johan Zaagsma, Edo Vellenga, and Henk F. Kauffman

Divisions of Allergology, Pulmonology, Molecular Pharmacology, and Hematology, Department of Internal Medicine and University Centre for Pharmacy, University of Groningen, Groningen, The Netherlands

Cytokine gene expression in T lymphocytes is a strictly regulated process, involving both stimulatory and inhibitory signals. beta -Adrenoceptor (beta AR) agonists are widely used in the treatment of asthma and are able to induce an inhibitory signal on immunological responses after binding to their specific receptors. In this study, the characterization of beta AR subtype(s) (beta 1, beta 2, and beta 3) involved in the regulation of interleukin (IL)-3, IL-4, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon-gamma (IFN-gamma ) mRNA accumulation was studied by using various beta AR agonists and antagonists. Concanavalin A (Con A)-induced IFN-gamma , GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective beta AR agonist isoproterenol and by the selective beta 2AR agonist fenoterol. IL-4 mRNA accumulation was not susceptible to beta AR stimulation. The observed inhibition on IFN-gamma , GM-CSF, and IL-3 mRNA was blocked by the selective beta 2AR antagonist ICI 118,551 (10-6 M) and by timolol (10-6 M), a nonselective antagonist. The selective beta 1AR antagonist atenolol (0.3 × 10-6 M) did not have any effect. Secretion of GM-CSF protein in the presence of increasing concentrations of isoproterenol followed a similar pattern as observed for GM-CSF mRNA. In addition, the beta AR-mediated inhibition of IFN-gamma , GM-CSF, and IL-3 mRNA accumulation and GM-CSF protein secretion were related to the accumulation of intracellular cyclic adenosine monophosphate (cAMP) levels. Although beta 3AR mRNA was detectable in Con A-activated T lymphocytes, we could not demonstrate a functional activity in the regulation of cytokine expression: the beta 3AR agonist BRL 37344 had no effect on the accumulation of the studied cytokine mRNAs, and did not significantly affect cellular cAMP levels. These data demonstrate that beta -agonist-induced inhibition of IFN-gamma , GM-CSF, and IL-3 mRNA accumulation is solely mediated by beta 2-adrenoceptors.




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