Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation

Interleukin-l (IL-1) is an important mediator in the mechanisms underlying the immune and inflammatory responses. It has pleiotropic effects in host defense and, when present in high concentrations, participates in the development of pathological processes. IL-1 is the most potent cytokine in the ac...

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Autor principal: Pereda, M.P
Otros Autores: Castro, C.P, Costas, M., Nahmod, V.E, Stalla, G.K, Holsboer, F., Arzt, E.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1996
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024 7 |2 scopus  |a 2-s2.0-12644271901 
024 7 |2 cas  |a dexamethasone, 50-02-2; hydrocortisone, 50-23-7; mifepristone, 84371-65-3; Endotoxins; Glucocorticoids; Interleukin-1; Lipopolysaccharides 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
100 1 |a Pereda, M.P. 
245 1 0 |a Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation 
260 |c 1996 
270 1 0 |m Arzt, E.; Instituto de Investigaciones Médicas, Facultad de Medicina, Universidad de Buenos Aires, Donato Alvarez 3150, Argentina 
506 |2 openaire  |e Política editorial 
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504 |a Ersson, L.B., Bjork, L., Dinarello, C.A., Towbin, H., Ersson, U., Lipopolysaccharidc induces human interleukin-1 receptor antagonist and interleukin-1 production in the same cell (1992) Eurj Immunol, 22, pp. 2617-2623 
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504 |a Bcscdovsky, H., Del Rev, A., Sorkin, E., Dinarcl-Lo, C.A., Immunorcgulatory feedback between interleukin-1 and glucocorticoid hormones (1986) Science, 233, pp. 652-654 
504 |a Arzt, E., Sauer, J., Pollmacher, T., Labeur, M., Llols-Bocr, F., Reul, J., Stalla, G.K., Glucocorticoids suppress interleukin-1 receptor antagonist synthesis follow ing induction by endotoxin (1994) Endocrinology, 134, pp. 672-677 
504 |a Sauer, J., Castren, M., Hopfner, U., Holsboer, F., Stalla, G.K., Arzt, E., Inhibition of lipopolysac-charide-induccd monocyte interleukin-1 rcccptor antagonist synthesis by cortisol: Involvement of the mineralocorticoid receptor (1996) J Clin Endocrinol Metab, 81, pp. 73-79 
504 |a Arzt, E., Fernández, C.S., Finocchiaro, L., Criscuolo, M., Diaz, A., Finkielman, S., Nahmod, V.E., Immunomodulation by indolcamincs: Serotonin and melatonin action on DNA and interferon gamma synthesis by human peripheral blood mononuclear cells (1988) J Clin Immunol, 8, pp. 513-519 
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504 |a Knudsen, P.J., Dinarello, C.A., Strom, T.B., Prostaglandins posttranseriptionally inhibit mono-cvtc expression of interleukin I activity by increasing intracellular cyclic adenosine monophosphate (1986) J Immunol, 137, pp. 3189-3194 
520 3 |a Interleukin-l (IL-1) is an important mediator in the mechanisms underlying the immune and inflammatory responses. It has pleiotropic effects in host defense and, when present in high concentrations, participates in the development of pathological processes. IL-1 is the most potent cytokine in the activation of the hypothalamic-pituitary-adrenal axis during infection and therefore leads to a glucocorticoid increase. Glucocorticoids in a feedback loop inhibit the production of IL-1 induced by endotoxin. IL-1 also induces its own synthesis. In this report, we examine the role of glucocorticoids in the regulation of IL-1 autoregulatory induction in human monocytes at the level of IL-1 protein production and mRNA accumulation. Using recombinant IL1 receptor antagonist we established that endogenously produced IL-1 affects induction of IL-1βprotein by lipopolysaccharide (LPS) at the level of mRNA expression. The inhibition of LPS-stimulated IL-1βproduction and mRNA expression by glucocorticoids (dexamethasone and Cortisol) reaches the same level with glucocorticoids alone or in combination with rIL-1ra. IL-1βmRNA induced by exogenously added IL-1βwas also inhibited by glucocorticoids. These results indicate that glucocorticoids inhibit the autoregulatory loop of IL-1 in LPS-stimulated monocytes and constitute a mechanism for controlling IL-1 feedback stimulation. © 1996 S. Karger AG, Basel.  |l eng 
593 |a Instituto de Investigaciones Médicas, Facultad de Medicina, Universidad de Buenos Aires, Argentina 
593 |a Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany 
593 |a Departamento de Biologia, FCEN, Universidad de Buenos Aires, Argentina 
690 1 0 |a ENDOTOXIN 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a INTERLEUKIN-L 
690 1 0 |a MONOCYTES 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a GLUCOCORTICOID 
690 1 0 |a HYDROCORTISONE 
690 1 0 |a INTERLEUKIN 1 RECEPTOR BLOCKING AGENT 
690 1 0 |a INTERLEUKIN 1BETA 
690 1 0 |a LIPOPOLYSACCHARIDE 
690 1 0 |a MESSENGER RNA 
690 1 0 |a MIFEPRISTONE 
690 1 0 |a ADULT 
690 1 0 |a ARTICLE 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a MONOCYTE 
690 1 0 |a NORMAL HUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a CELLS, CULTURED 
690 1 0 |a DOSE-RESPONSE RELATIONSHIP, DRUG 
690 1 0 |a ENDOTOXINS 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a HUMANS 
690 1 0 |a INTERLEUKIN-1 
690 1 0 |a LIPOPOLYSACCHARIDES 
690 1 0 |a MONOCYTES 
650 1 7 |2 spines  |a HOMEOSTASIS 
653 0 0 |a ru 38486, roussel uclaf, France 
700 1 |a Castro, C.P. 
700 1 |a Costas, M. 
700 1 |a Nahmod, V.E. 
700 1 |a Stalla, G.K. 
700 1 |a Holsboer, F. 
700 1 |a Arzt, E. 
773 0 |d 1996  |g v. 3  |h pp. 227-232  |k n. 4  |p NeuroImmunomodulation  |x 10217401  |t NeuroImmunoModulation 
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