Expression profiles of human 11β-hydroxysteroid dehydrogenases type 1 and type 2 in inflammatory bowel diseases

Inflammatory bowel diseases such as Crohn's disease (CD) and ulcerative colitis (UC) are characterized by an increase in pro-inflammatory cytokines. On the other hand, endogenous cortisol is regarded as physiological compound to combat inflammation. The local activation of glucocorticoids is me...

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Published in:Molecular and cellular endocrinology Vol. 301; no. 1; pp. 104 - 108
Main Authors: Stegk, J.P., Ebert, B., Martin, H.-J., Maser, E.
Format: Journal Article
Language:English
Published: Elsevier Ireland Ltd 25-03-2009
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Summary:Inflammatory bowel diseases such as Crohn's disease (CD) and ulcerative colitis (UC) are characterized by an increase in pro-inflammatory cytokines. On the other hand, endogenous cortisol is regarded as physiological compound to combat inflammation. The local activation of glucocorticoids is mediated by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) which increases cortisol, and 11β-HSD2 which decreases cortisol concentrations. We hypothesized that in inflamed tissues of patients suffering from inflammatory bowel diseases 11β-HSD1 is upregulated whereas 11β-HSD2 is downregulated. By using quantitative real-time PCR, we investigated the transcription levels of 11β-HSD1 and 11β-HSD2 in patients diagnosed with CD or UC. Expression of 11β-HSD1 was significantly elevated in inflamed tissue compared to non-inflamed colonic tissue in both, CD (2.7-fold) and UC (3.8-fold), whereas 11β-HSD2 expression was decreased in the same samples. In both diseases, male patients showed a more pronounced upregulation of 11β-HSD1 (CD: 4.8-fold, UC: 6.5-fold) compared to females (CD: 1.8-fold, UC: 1.8-fold), a fact which might be due to the higher levels of circulating anti-inflammatory estrogens in women. Our data support the hypothesis that both enzymes play a crucial role in inflammation by affecting local tissue ratios between active and inactive glucocorticoids.
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ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2008.10.030