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: | , , , , , , |
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| Formato: | JOUR |
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_10217401_v3_n4_p227_Pereda |
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| Sumario: | 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. |
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