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Modulation by Cytokines of Glucocorticoid Action
Author(s) -
ANGELI ALBERTO,
MASERA ROSA GABRIELLA,
SARTORI MARIA LUISA,
FORTUNATI NICOLETTA,
RACCA SILVIA,
DOVIO ANDREA,
STAURENGHI ANTONIO,
FRAIRIA ROBERTO
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07641.x
Subject(s) - autocrine signalling , cytokine , glucocorticoid receptor , glucocorticoid , receptor , proinflammatory cytokine , immune system , chemistry , microbiology and biotechnology , endocrinology , interleukin , medicine , biology , inflammation , immunology
Glucocorticoids (GC) are potent modulators of the inflammatory response. Their effects serve to down‐regulate the inflammatory response and are mediated by genomic pathways that follow the interaction with specific receptors (glucocorticoid receptors, GR). Interleukin (IL)‐1, IL‐2, and IL‐6 are able to increase GC secretion by enhancing synthesis and release of CRH and ACTH. Cytokine effects upon steroidogenesis also occur at the adrenal level. The role of cytokines as modulators of GR has received scarce attention. IL‐1 has been shown to up‐regulate GR mRNA expression in hypothalamic CRH secreting cells. On the other hand, macrophage migration inhibitory factor (MIF), a T‐cell product inducible by inflammatory substances including other cytokines, counterregulates GC action within the immune system. Besides immunocytes and neurons, bone cells are a sensitive target for GC and cytokines. We have found that IL‐2 and IL‐6 up‐regulate remarkably the number of GR binding sites and the expression of GR mRNA in peripheral blood mononuclear cells and in osteoblast‐like Saos‐2 cells. Available data suggest that inflammatory cytokines have both direct and indirect effects on GC action at the target level. Autocrine‐induced transcription of GR in immunocytes and/or osteoblasts could be a mechanism that restrains excess cytokine production.