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Tumor Necrosis Factor and Interleukin 1β Enhance the Cortisone/Cortisol Shuttle

From the Division of Nephrology, University Hospital of Berne, 3010 Berne, Switzerland

Endogenously released or exogenously administered glucocorticosteroids are relevant hormones for controlling inflammation. Only 11β-hydroxy glucocorticosteroids, but not 11-keto glucocorticosteroids, activate glucocorticoid receptors. Since we found that glomerular mesangial cells (GMC) express 11β-hydroxysteroid dehydrogenase 1 (11β-OHSD1), which interconverts 11-keto glucocorticosteroids into 11β-hydroxy glucocorticosteroids (cortisone/cortisol shuttle), we explored whether 11β-OHSD1 determines the antiinflammatory effect of glucocorticosteroids. GMC exposed to interleukin (IL)-1β or tumor necrosis factor (TNF-) release group II phospholipase A2 (PLA2), a key enzyme producing inflammatory mediators. 11β-hydroxy glucocorticosteroids inhibited cytokine-induced transcription and release of PLA2 through a glucocorticoid receptor–dependent mechanism. This inhibition was enhanced by inhibiting 11β-OHSD1. Interestingly, 11-keto glucocorticosteroids decreased cytokine-induced PLA2 release as well, a finding abrogated by inhibiting 11β-OHSD1. Stimulating GMC with IL-1β or TNF- increased expression and reductase activity of 11β-OHSD1. Similarly, this IL-1β– and TNF-–induced formation of active 11β-hydroxy glucocorticosteroids from inert 11-keto glucocorticosteroids by the 11β-OHSD1 was shown in the Kiki cell line that expresses the stably transfected bacterial β-galactosidase gene under the control of a glucocorticosteroids response element. Thus, we conclude that 11β-OHSD1 controls access of 11β-hydroxy glucocorticosteroids and 11-keto glucocorticosteroids to glucocorticoid receptors and thus determines the anti-inflammatory effect of glucocorticosteroids. IL-1β and TNF- upregulate specifically the reductase activity of 11β-OHSD1 and counterbalance by that mechanism their own proinflammatory effect.

¹Abbreviations used in this paper: dCTP, desoxy CTP; GA, glycyrrhetinic acid; GAPDH, glyceraldehydephosphate dehydrogenase; GMC, glomerular mesangial cells; mRNA, messenger RNA; NAD, nicotinamide adenine dinucleotide; NADP, NAD phosphate; NADPH, reduced form of NADP; OHSD, hydroxysteroid dehydrogenase; PLA2, phospholipase A2; RT-PCR, reverse transcribed PCR.

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