Abstract:
The interleukin-1 (IL-1) system is constituted by IL-1 alpha and IL-1 β and IL-1 receptor antagonist (IL-1ra) that bind the same IL-1 receptors. Hypothalamic-pituitary-adrenal axis hormones are major mediators of the neuroendocrine control over immune function. Corticotropin-releasing hormone (CRH) is produced in peripheral inflammatory sites; its direct effects on inflammatory cytokine synthesis, however, remain unclear. We have studied the effects of CRH (0.1-100 nM) on IL-1 β and IL-1ra expression by human peripheral monocytes in culture activated with different doses of lipopolysaccharide (LPS). In the absence of LPS, CRH up-regulated IL-1ra and IL-1 β messenger RNA expression as well as protein synthesis. No significant changes were observed with low doses of LPS (1 ng/ml). In contrast, in combination with high doses of LPS (1 μ/ml), CRH caused inhibition of IL-1ra and IL-1 β transcription and secretion. The CRH effects were blocked by its antagonist alpha-helical CRH and mediated by intracellular cAMP. These data indicate that CRH modulates the IL-1 system; depending on the state of activation of the monocyte, CRH exerts an inhibitory control on the activated cell and a stimulatory action on the resting monocyte. © 1995 by The Endocrine Society.
Registro:
Documento: |
Artículo
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Título: | Corticotropin-releasing hormone differentially modulates the interleukin-1 system according to the level of monocyte activation by endotoxin |
Autor: | Pereda, M.P.; Sauer, J.; Castro, C.P.; Finkielman, S.; Stalla, G.K.; Holsboer, F.; Arzt, E. |
Filiación: | Instituto de Investigaciones Médicas, Universidad de Buenos Aires, Buenos Aires, Argentina Departamento de Biología-FCEN, Universidad de Buenos Aires, Buenos Aires, Argentina Max-Planck Institute of Psychiatry, Clinical Institute, Munich, 80804, Germany
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Palabras clave: | corticotropin releasing factor; interleukin 1; interleukin receptor; article; corticotropin release; human; human cell; hypothalamus hypophysis adrenal system; leukocyte activation; priority journal; protein synthesis; Cells, Cultured; Corticotropin-Releasing Hormone; Cyclic AMP; Gene Expression Regulation; Human; Interleukin-1; Lipopolysaccharides; Monocytes; RNA, Messenger; Sialoglycoproteins; Support, Non-U.S. Gov't |
Año: | 1995
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Volumen: | 136
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Número: | 12
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Página de inicio: | 5504
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Página de fin: | 5510
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DOI: |
http://dx.doi.org/10.1210/endo.136.12.7588301 |
Título revista: | Endocrinology
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Título revista abreviado: | Endocrinology
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ISSN: | 00137227
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CAS: | corticotropin releasing factor, 9015-71-8; Corticotropin-Releasing Hormone, 9015-71-8; Cyclic AMP, 60-92-4; interleukin 1 receptor antagonist protein; Interleukin-1; Lipopolysaccharides; RNA, Messenger; Sialoglycoproteins
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Registro: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v136_n12_p5504_Pereda |
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Citas:
---------- APA ----------
Pereda, M.P., Sauer, J., Castro, C.P., Finkielman, S., Stalla, G.K., Holsboer, F. & Arzt, E.
(1995)
. Corticotropin-releasing hormone differentially modulates the interleukin-1 system according to the level of monocyte activation by endotoxin. Endocrinology, 136(12), 5504-5510.
http://dx.doi.org/10.1210/endo.136.12.7588301---------- CHICAGO ----------
Pereda, M.P., Sauer, J., Castro, C.P., Finkielman, S., Stalla, G.K., Holsboer, F., et al.
"Corticotropin-releasing hormone differentially modulates the interleukin-1 system according to the level of monocyte activation by endotoxin"
. Endocrinology 136, no. 12
(1995) : 5504-5510.
http://dx.doi.org/10.1210/endo.136.12.7588301---------- MLA ----------
Pereda, M.P., Sauer, J., Castro, C.P., Finkielman, S., Stalla, G.K., Holsboer, F., et al.
"Corticotropin-releasing hormone differentially modulates the interleukin-1 system according to the level of monocyte activation by endotoxin"
. Endocrinology, vol. 136, no. 12, 1995, pp. 5504-5510.
http://dx.doi.org/10.1210/endo.136.12.7588301---------- VANCOUVER ----------
Pereda, M.P., Sauer, J., Castro, C.P., Finkielman, S., Stalla, G.K., Holsboer, F., et al. Corticotropin-releasing hormone differentially modulates the interleukin-1 system according to the level of monocyte activation by endotoxin. Endocrinology. 1995;136(12):5504-5510.
http://dx.doi.org/10.1210/endo.136.12.7588301