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School of Biomedical Sciences, Australia Zoo Wildlife Hospital, Landscape Ecology and Conservation Group, Office of Environment and Heritage NSW, School of Biology and Biotechnology, The University of Queensland, St Lucia, Queensland 4072, Australia
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release of glucocorticoid (GC) hormones (mainly cortisol or corticosterone in mammals) by the adrenal cortex ( Seyle 1935 , Axelrod & Reisine 1984 , Mostl & Palme 2002 , Stewart 2003 ). Short-term GC secretions, resulting from acute stress (e
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Introduction Bone loss and fractures resulting from glucocorticoid (GC) therapy is the most prevalent form of secondary osteoporosis ( Van Staa et al . 2000 , Angeli et al . 2006 ). Skeletal health and repair depends on
Faculty of Medical and Human Sciences, Faculty of Life Sciences, Faculty of Medical and Human Sciences, School of Medicine
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Faculty of Medical and Human Sciences, Faculty of Life Sciences, Faculty of Medical and Human Sciences, School of Medicine
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Introduction Glucocorticoids (GC) act through the GC receptor (GR), a member of the nuclear receptor superfamily of ligand-regulated transcription factors ( Hollenberg et al . 1985 , Weinberger et al . 1985 , 1987 , Perlmann & Evans 1997
Department of Pediatrics, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA
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183 583 – 590 . ( doi:10.1111/j.1432-1033.1989.tb21087.x ) Dong Y Pan JS Zhang L 2013 Myostatin suppression of Akirin1 mediates glucocorticoid-induced satellite cell dysfunction . PLoS ONE 8 e58554 . ( doi:10.1371/journal.pone.0058554
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Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
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Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
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Introduction Glucocorticoid (GC) hormones, like cortisol, are produced and released from the zona fasciculata of the adrenal gland under the control of a prototypic neuroendocrine feedback system of the hypothalamic–pituitary–adrenal (HPA) axis. GCs
Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Department of Endocrinology, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 5TT, UK
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Introduction The cellular actions of glucocorticoids (GCs) are largely mediated through interactions with the glucocorticoid receptor (GR), a nuclear receptor that is found in its inactive form within the cytoplasm. Ligand
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Introduction
Increased glucocorticoid secretion is a key feature of the stress response, serving to mobilise energy substrates, inhibit non-vital processes and restore stress effector systems. However, chronic glucocorticoid excess (in Cushing's disease or during pharmacotherapy) is associated with a broad spectrum of deleterious effects including diabetes mellitus, reproductive failure, hypertension, osteoporosis, immunosuppression, myopathy, growth impairment and, not least, affective and cognitive dysfunction. Clearly therefore, the autoregulatory (negative feedback) actions of glucocorticoids upon the hypothalamic-pituitary-adrenal (HPA) axis are of crucial importance.
Glucocorticoids act, in large part, by binding to intracellular receptors. There are two types, mineralocorticoid (MR, type I) and glucocorticoid (GR, type II) (McEwen et al. 1986) receptors. Ligand-activated receptors function as nuclear transcription factors, attaching to specific DNA sequences and regulating target gene expression. Interactions with other nuclear factors, notably AP-1 (Pfahl 1993) and cyclic AMP response element binding protein (Stauber et al. 1992), may also occur and modulate
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Abstract
Glucocorticoids are among the most potent anti-inflammatory agents that can be used in the treatment of rhinitis. Their mechanisms of action are multiple and complex and a number of reports describe significant systemic effects of locally administered glucocorticoids. In order to evaluate the short-term systemic effects of intranasally administered glucocorticoids, 14 normal healthy subjects were treated with two doses of either budesonide (BUD) or fluticasone propionate (FP) for 2 weeks. Before treatment, at regular intervals during the treatment, 1 week and finally 6 weeks after termination of treatment, the effects on glucocorticoid receptor (GR) and methallothionein (MTIIa) mRNA expression levels were examined in peripheral lymphocytes using a solution hybridization assay. Serum cortisol, osteocalcin and urinary cortisol levels were also determined. An insulin tolerance test (ITT) was performed at the end of the second week of treatment and at the end of the 6-week washout period with no statistically significant change in cortisol response. In peripheral lymphocytes, GR mRNA levels were significantly down-regulated. MTIIa mRNA levels increased significantly. Serum osteocalcin decreased significantly during treatment with both BUD and FP. Serum cortisol decreased after 1 week of treatment whereas urinary cortisol was not affected until the second week of treatment. In conclusion, intranasal glucocorticoids at clinically recommended doses have not only significant systemic effects on adrenal function, but also have an effect on specific gene expression in peripheral lymphocytes. These effects are receptor-dependent, reversible, and according to serum and urinary cortisol levels and ITT, leave the hypothalamic-pituitary-adrenal function intact. Finally, these short-term systemic effects were not associated with any of the noticeable side-effects usually observed during long-term treatment with glucocorticoids.
Journal of Endocrinology (1995) 144, 301–310
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The interplay between the endocrine and immune systems has come into focus in recent years with the insight that endocrine parameters may affect susceptibility to both auto-immune and infectious diseases. Our interest in immunoendocrine regulation led us to investigate the effects of glucocorticoids on Herpes simplex virus type 1 (HSV-1) infections. Glucocorticoids used to treat inflammatory conditions are not yet recommended for HSV-1 therapy, since they have been reported to prolong viral shedding both in vivo and in vitro. Here we report that glucocorticoids did not alter the viral yield in human gingival fibroblast (HGF) cell culture when glucocorticoid treatment and viral infection occured simultaneously, but the viral yield increased when cells were treated with the glucocorticoid dexamethasone (dex) prior to viral infection. We found that viral infection in our primary cell system increased NF-kappaB levels and DNA binding. In addition, the amount of glucocorticoid receptor (GR) increased following viral infection, and HSV-1 infection as such could induce glucocorticoid-driven transcription of a reporter gene in human embryo kidney (HEK) 293 cells stably transfected with GR. Dex treatment did not affect HSV-1-induced binding of p65 to an NF-kappaB element in an electrophoretic mobility shift assay, and acyclovir was still efficient as an anti-viral drug in the presence of dex. Further studies of the observed effects of HSV-1 infection and glucocorticoid treatment on GR and NF-kappaB regulation could give insights into the immunoendocrine mechanisms important for defence and therapy against viral infections.
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in adrenal function (for reviews see Gluckman & Hanson (2004) and Seckl & Holmes (2007) ). Nutritional perturbations, placental dysfunction and fetal glucocorticoid excess are all recognized as key determinants of a poor fetal environment, and
