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Titolo:
Glucocorticoids ablate IL-1 beta-induced beta-adrenergic hyporesponsiveness in human airway smooth muscle cells
Autore:
Moore, PE; Laporte, JD; Gonzalez, S; Moller, W; Heyder, J; Panettieri, RA; Shore, SA;
Indirizzi:
Harvard Univ, Sch Publ Hlth, Physiol Program, Dept Environm Hlth, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Dept Environm Hlth, Boston, MA 02115 USA GSF, Natl Res Ctr Environm & Hlth, Inst Inhalat Biol, D-85764 Oberschleissheim, Germany GSF Oberschleissheim Germany D-85764 , D-85764 Oberschleissheim, Germany Univ Penn, Dept Med, Div Pulm & Crit Care, Philadelphia, PA 19102 USA UnivPenn Philadelphia PA USA 19102 Crit Care, Philadelphia, PA 19102 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 5, volume: 277, anno: 1999,
pagine: L932 - L942
SICI:
1040-0605(199911)277:5<L932:GAIBBH>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR-KAPPA-B; CYCLO-OXYGENASE-2; INDUCTION; CYTOKINES; RECEPTOR; TRANSCRIPTION; EXPRESSION; ALPHA; GENE; INTERLEUKIN-1-BETA;
Keywords:
interleukin-1 beta; beta(2)-adrenergic receptor; magnetic twisting cytometry; adenosine 3 ',5 '-cyclic monophosphate; cyclooxygenase-2; prostaglandin E-2; nuclear factor-kappa B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Shore, SA Harvard Univ, Sch Publ Hlth, Physiol Program, Dept Environm Hlth, 665 Huntington Ave, Boston, MA 02115 USA Harvard Univ 665 Huntington Ave Boston MA USA 02115 MA 02115 USA
Citazione:
P.E. Moore et al., "Glucocorticoids ablate IL-1 beta-induced beta-adrenergic hyporesponsiveness in human airway smooth muscle cells", AM J P-LUNG, 277(5), 1999, pp. L932-L942

Abstract

We have previously reported that interleukin (IL)-1 beta decreases responsiveness of cultured human airway smooth muscle (HASM) cells to beta-agonists. The purpose of this study was to determine whether glucocorticoids inhibit this IL-1 beta 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 beta (20 ng/ml)-treated cells. In addition, Dex had no effect on Iso-stimulated cAMP formation in control cells but prevented the IL-1 beta-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 beta-induced hyporesponsivenessto PGE(2) stimulation. In contrast, neither IL-1 beta nor glucocorticoids had any effect on cell stiffness responses to dibutyryl cAMP. We have previously reported that the IL-1 beta effect on beta-adrenergic responsiveness is mediated through cyclooxygenase-2 expression and prostanoid formation. Consistent with these observations, IL-lp-induced cyclooxygenase-2 expression was virtually abolished by FP at concentrations of 10(-10) M and greater,with a resultant decrease in PGE2 formation. However, Dex did not inhibit IL-1 beta-induced nuclear translocation of nuclear factor-kappa B or activator protein-1 in HASM cells. In summary, our results indicate that, in HASMcells, glucocorticoids alone do not alter responses to beta-agonists but do inhibit IL-1 beta-induced beta-adrenergic hyporesponsiveness. Glucocorticoids mediate this effect by inhibiting prostanoid formation but without altering nuclear factor-kappa B or activator protein-1 translocation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 19:10:23