PMID: 11897990Mar 19, 2002Paper

Modulation of T-cell function by (R)- and (S)-isomers of albuterol: anti-inflammatory influences of (R)-isomers are negated in the presence of the (S)-isomer

The Journal of Allergy and Clinical Immunology
Dawn BaramkiLarry Borish

Abstract

beta(2)-Adrenergic agonists interact with specific receptors on T lymphocytes to mediate anti-inflammatory activities. However, anti-inflammatory effects are not observed when beta(2)-adrenergic agonists are administered in vivo as racemates. We hypothesized that anti-inflammatory influences are mediated by the (R)-isomer and are masked in the additional presence of the (S)-isomer. Antigen-specific T-cell lines were generated in the presence of recombinant human IL-2 and tetanus with or without varying concentrations of (R)- and (S)-isomers of albuterol alone or in combination. Parallel lines were generated in the presence of propranolol. Cells were briefly pulsed with PHA and evaluated for proliferation, apoptosis, and cytokine secretion. (R)-Albuterol significantly inhibited T-cell proliferation (77.0% +/- 9.7% of control at 10(-8) mol/L and 61.1% +/- 9.0% at 10(-7) mol/L). No influence was observed with (S)-albuterol alone. However, the addition of (S)-albuterol to (R)-albuterol mediated a dose-dependent increase in proliferation. At equivalent concentrations of the 2 isomers, proliferation was unchanged from the control, whereas at 10(-6) mol/L (S)-albuterol, proliferation was enhanced. Both the inhibitory effects of (R)-al...Continue Reading

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