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-induced -adrenergic
hyporesponsiveness in human airway smooth muscle cells
1 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115; 2 GSF National Research Center for Environment and Health, Institute for Inhalation Biology, D-85764 Oberschleissheim, Germany; and 3 Pulmonary and Critical Care Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19102
We have previously reported that interleukin
(IL)-1
decreases responsiveness of cultured human airway smooth
muscle (HASM) cells to -agonists. The purpose of this study was to
determine whether glucocorticoids inhibit this IL-1
effect. Dexamethasone (Dex;
10
6 M) had no effect on
concentration-related decreases in cell stiffness in response to
isoproterenol (Iso) in control cells as measured by magnetic twisting
cytometry but prevented the decreased responsiveness to Iso observed in
IL-1 (20 ng/ml)-treated cells. In addition, Dex had no effect on
Iso-stimulated cAMP formation in control cells but prevented the
IL-1-induced reduction in Iso-stimulated cAMP formation. Similar
effects on cell stiffness and cAMP responses were seen after
pretreatment with the glucocorticoid fluticasone proprionate (FP). Dex
and FP also prevented IL-1-induced hyporesponsiveness to
PGE2 stimulation. In contrast,
neither IL-1 nor glucocorticoids had any effect on cell stiffness
responses to dibutyryl cAMP. We have previously reported that the
IL-1 effect on -adrenergic responsiveness is mediated through
cyclooxygenase-2 expression and prostanoid formation. Consistent with
these observations, IL-1-induced cyclooxygenase-2 expression was
virtually abolished by FP at concentrations of
1010 M and greater, with a
resultant decrease in PGE2
formation. However, Dex did not inhibit IL-1-induced nuclear
translocation of nuclear factor-
B or activator protein-1 in HASM
cells. In summary, our results indicate that, in HASM cells,
glucocorticoids alone do not alter responses to -agonists but do
inhibit IL-1-induced -adrenergic hyporesponsiveness.
Glucocorticoids mediate this effect by inhibiting prostanoid formation
but without altering nuclear factor-B or activator protein-1 translocation.
interleukin-1; 2-adrenergic receptor; magnetic
twisting cytometry; adenosine 3',5'-cyclic monophosphate; cyclooxygenase-2; prostaglandin
E2; nuclear factor-B
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