ArticleThe Journal of experimental medicine1997
Tumor necrosis factor alpha and interleukin 1beta enhance the cortisone/cortisol shuttle.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 181 citations in OpenAlex.
- A description of the elevation of pericardial cortisol: cortisone ratio in patients with tuberculous pericarditis.Frontiers in endocrinology · 2023Article
- Aging versus youth: Endocrine aspects of vulnerability for COVID-19.Reviews in endocrine & metabolic disorders · 2022Review
- Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.Neuroscience letters · 2019Review
- 11β-hydroxysteroid dehydrogenase-1 deficiency alters brain energy metabolism in acute systemic inflammation.Brain, behavior, and immunity · 2018Article
- Hepatic inflammation induced by high-fructose diet is associated with altered 11βHSD1 expression in the liver of Wistar rats.European journal of nutrition · 2014Article
- Elevated hepatic 11β-hydroxysteroid dehydrogenase type 1 induces insulin resistance in uremia.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Regulation of 11β-hydroxysteroid dehydrogenase type 1 and 7α-hydroxylase CYP7B1 during social stress.PloS one · 2014Article
- Evidence for glucocorticoid-mediated hypertension after uninephrectomy.Physiological reports · 2013Article
- 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.Physiological reviews · 2013Review
- Activated glucocorticoid and eicosanoid pathways in endometriosis.Fertility and sterility · 2012Article
- Synergistic induction of local glucocorticoid generation by inflammatory cytokines and glucocorticoids: implications for inflammation associated bone loss.Annals of the rheumatic diseases · 2010Article
- Impaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis.Journal of endocrinological investigation · 2010Article
- Glucocorticoid availability in colonic inflammation of rat.Digestive diseases and sciences · 2008Article
- 11beta-HSD1, inflammation, metabolic disease and age-related cognitive (dys)function.Neurochemical research · 2008Review
- Neuroendocrine-immune interactions in rheumatoid arthritis: mechanisms of glucocorticoid resistance.Neuroimmunomodulation · 2008Review
- DHEA induces 11 -HSD2 by acting on CCAAT/enhancer-binding proteins.Journal of the American Society of Nephrology : JASN · 2008Article
- Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas.British journal of cancer · 2005Article
- Epigenetic regulation of 11 beta-hydroxysteroid dehydrogenase type 2 expression.The Journal of clinical investigation · 2004Article
- Science review: mechanisms of impaired adrenal function in sepsis and molecular actions of glucocorticoids.Critical care (London, England) · 2004Review
- Annexin 1 (lipocortin 1) mimics inhibitory effects of glucocorticoids on testosterone secretion and enhances effects of interleukin-1beta.Endocrine · 2002Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenously released or exogenously administered glucocorticosteroids are relevant hormones for controlling inflammation. Only 11beta-hydroxy glucocorticosteroids, but not 11-keto glucocorticosteroids, activate glucocorticoid receptors. Since we found that glomerular mesangial cells (GMC) express 11beta-hydroxysteroid dehydrogenase 1 (11beta-OHSD1), which interconverts 11-keto glucocorticosteroids into 11beta-hydroxy glucocorticosteroids (cortisone/cortisol shuttle), we explored whether 11beta-OHSD1 determines the antiinflammatory effect of glucocorticosteroids. GMC exposed to interleukin (IL)-1beta or tumor necrosis factor alpha (TNF-alpha) release group II phospholipase A2 (PLA2), a key enzyme producing inflammatory mediators. 11beta-hydroxy glucocorticosteroids inhibited cytokine-induced transcription and release of PLA2 through a glucocorticoid receptor-dependent mechanism. This inhibition was enhanced by inhibiting 11beta-OHSD1. Interestingly, 11-keto glucocorticosteroids decreased cytokine-induced PLA2 release as well, a finding abrogated by inhibiting 11beta-OHSD1. Stimulating GMC with IL-1beta or TNF-alpha increased expression and reductase activity of 11beta-OHSD1. Similarly, this IL-1beta- and TNF-alpha-induced formation of active 11beta-hydroxy glucocorticosteroids from inert 11-keto glucocorticosteroids by the 11beta-OHSD1 was shown in the Kiki cell line that expresses the stably transfected bacterial beta-galactosidase gene under the control of a glucocorticosteroids response element. Thus, we conclude that 11beta-OHSD1 controls access of 11beta-hydroxy glucocorticosteroids and 11-keto glucocorticosteroids to glucocorticoid receptors and thus determines the anti-inflammatory effect of glucocorticosteroids. IL-1beta and TNF-alpha upregulate specifically the reductase activity of 11beta-OHSD1 and counterbalance by that mechanism their own proinflammatory effect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.