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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Autores principales: Páez Pereda, Marcelo, Perez Castro, Carolina Inés, Costas, Mónica Alejandra
Publicado: 1996
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v3_n4_p227_Pereda
http://hdl.handle.net/20.500.12110/paper_10217401_v3_n4_p227_Pereda
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spelling paper:paper_10217401_v3_n4_p227_Pereda2023-06-08T16:00:02Z Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation Páez Pereda, Marcelo Perez Castro, Carolina Inés Costas, Mónica Alejandra Endotoxin Glucocorticoids Interleukin-l Monocytes dexamethasone glucocorticoid hydrocortisone interleukin 1 receptor blocking agent interleukin 1beta lipopolysaccharide messenger rna mifepristone adult article human human cell monocyte normal human priority journal Cells, Cultured Dose-Response Relationship, Drug Endotoxins Glucocorticoids Homeostasis Humans Interleukin-1 Lipopolysaccharides Monocytes 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. Fil:Pereda, M.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Castro, C.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Costas, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 1996 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v3_n4_p227_Pereda http://hdl.handle.net/20.500.12110/paper_10217401_v3_n4_p227_Pereda
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Endotoxin
Glucocorticoids
Interleukin-l
Monocytes
dexamethasone
glucocorticoid
hydrocortisone
interleukin 1 receptor blocking agent
interleukin 1beta
lipopolysaccharide
messenger rna
mifepristone
adult
article
human
human cell
monocyte
normal human
priority journal
Cells, Cultured
Dose-Response Relationship, Drug
Endotoxins
Glucocorticoids
Homeostasis
Humans
Interleukin-1
Lipopolysaccharides
Monocytes
spellingShingle Endotoxin
Glucocorticoids
Interleukin-l
Monocytes
dexamethasone
glucocorticoid
hydrocortisone
interleukin 1 receptor blocking agent
interleukin 1beta
lipopolysaccharide
messenger rna
mifepristone
adult
article
human
human cell
monocyte
normal human
priority journal
Cells, Cultured
Dose-Response Relationship, Drug
Endotoxins
Glucocorticoids
Homeostasis
Humans
Interleukin-1
Lipopolysaccharides
Monocytes
Páez Pereda, Marcelo
Perez Castro, Carolina Inés
Costas, Mónica Alejandra
Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
topic_facet Endotoxin
Glucocorticoids
Interleukin-l
Monocytes
dexamethasone
glucocorticoid
hydrocortisone
interleukin 1 receptor blocking agent
interleukin 1beta
lipopolysaccharide
messenger rna
mifepristone
adult
article
human
human cell
monocyte
normal human
priority journal
Cells, Cultured
Dose-Response Relationship, Drug
Endotoxins
Glucocorticoids
Homeostasis
Humans
Interleukin-1
Lipopolysaccharides
Monocytes
description 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.
author Páez Pereda, Marcelo
Perez Castro, Carolina Inés
Costas, Mónica Alejandra
author_facet Páez Pereda, Marcelo
Perez Castro, Carolina Inés
Costas, Mónica Alejandra
author_sort Páez Pereda, Marcelo
title Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
title_short Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
title_full Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
title_fullStr Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
title_full_unstemmed Glucocorticoids Inhibit the Autoregulatory Induction of lnterleukin-1 in Monocytes after Endotoxin Stimulation
title_sort glucocorticoids inhibit the autoregulatory induction of lnterleukin-1 in monocytes after endotoxin stimulation
publishDate 1996
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10217401_v3_n4_p227_Pereda
http://hdl.handle.net/20.500.12110/paper_10217401_v3_n4_p227_Pereda
work_keys_str_mv AT paezperedamarcelo glucocorticoidsinhibittheautoregulatoryinductionoflnterleukin1inmonocytesafterendotoxinstimulation
AT perezcastrocarolinaines glucocorticoidsinhibittheautoregulatoryinductionoflnterleukin1inmonocytesafterendotoxinstimulation
AT costasmonicaalejandra glucocorticoidsinhibittheautoregulatoryinductionoflnterleukin1inmonocytesafterendotoxinstimulation
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