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Titolo:
Signal transduction in smooth muscle - Selected contribution: Synergism between TNF-alpha and IL-1 beta in airway smooth muscle cells: implications for beta-adrenergic responsiveness
Autore:
Moore, PE; Lahiri, T; Laporte, JD; Church, T; Panettieri, RA; Shore, SA;
Indirizzi:
Harvard Univ, Sch Publ Hlth, Physiol Program, Boston, MA 02115 USA HarvardUniv Boston MA USA 02115 h, Physiol Program, Boston, MA 02115 USA Univ Penn, Sch Med, Dept Med, Div Pulm & Crit Care, Philadelphia, PA 19104USA Univ Penn Philadelphia PA USA 19104 Crit Care, Philadelphia, PA 19104USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 3, volume: 91, anno: 2001,
pagine: 1467 - 1474
SICI:
8750-7587(200109)91:3<1467:STISM->2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; MESSENGER-RNA; DIFFERENTIAL REGULATION; ADRENOCEPTOR AGONISTS; GENE-EXPRESSION; MESANGIAL CELLS; INTERLEUKIN-1-BETA; CYCLO-OXYGENASE-2; CYTOKINES;
Keywords:
isoproterenol; cyclooxygenase-2; mitogen-activated protein kinase; nuclear factor-kappa B; magnetic twisting cytometry; interleukin-1 beta; tumor necrosis factor-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Shore, SA Harvard Univ, Sch Publ Hlth, Physiol Program, 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., "Signal transduction in smooth muscle - Selected contribution: Synergism between TNF-alpha and IL-1 beta in airway smooth muscle cells: implications for beta-adrenergic responsiveness", J APP PHYSL, 91(3), 2001, pp. 1467-1474

Abstract

In human cultured airway smooth muscle cells, interleukin (IL)-1 beta increases cyclooxygenase (COX)-2 expression and PGE(2) release, ultimately resulting in decreased beta -adrenergic responsiveness. In this study, we aimedto determine whether tumor necrosis factor-alpha (TNF-alpha) synergizes with IL-1 beta in the induction of these events. TNF-alpha alone, at concentrations up to 10 ng/ml, had no effect on COX-2 protein expression; at concentrations as low as 0.1 ng/ml, it significantly enhanced the ability of IL-1beta (0.2 ng/ml) to induce COX-2 and to increase PGE(2) release. IL-1 betaand TNF-alpha in combination also significantly enhanced COX-2 promoter activity, indicating that synergism between the cytokines is mediated at the level of gene transcription. Although IL-1 beta and TNF-alpha each increased nuclear factor-kappaB activation and induced extracellular regulated kinase and p38 phosphorylation, combined administration of the cytokines did not enhance either nuclear factor-kappaB or mitogen-activated protein kinase activation. Combined administration of IL-1 beta (0.2 ng/ml) and TNF-alpha (0.1 or 1.0 ng/ml) reduced the ability of isoproterenol to decrease human airway smooth muscle cell stiffness, as measured by magnetic twisting cytometry, even though individually these cytokines, at these concentrations, hadno effect on isoproterenol responses. Treatment with the selective COX-2 inhibitor NS-398 abolished the synergistic effects of TNF-alpha and IL-1 beta on beta -adrenergic responsiveness. Our results indicate that low concentrations of IL-1 beta and TNF-alpha synergize to promote beta -adrenergic hyporesponsiveness and that effects on COX-2 expression and PGE(2) are responsible for these events. The data suggest that the simultaneous release in the airway, of even very small amounts of cytokines, can have important functional consequences.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 20:49:27