Altered Endocrine and Autocrine Metabolism of Vitamin D in a Mouse Model of Gastrointestinal Inflammation (original) (raw)

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1Department of Orthopaedic Surgery (N.L., R.F.C., V.L., J.S.A., M.H.), UCLA, Los Angeles, California 90095

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3Division of Endocrinology, Diabetes and Metabolism (L.N., S.R., S.W.), Burns and Allen Research Center, Cedars-Sinai Medical Center, David Geffen School of Medicine, Los Angeles, California 90048

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1Department of Orthopaedic Surgery (N.L., R.F.C., V.L., J.S.A., M.H.), UCLA, Los Angeles, California 90095

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1Department of Orthopaedic Surgery (N.L., R.F.C., V.L., J.S.A., M.H.), UCLA, Los Angeles, California 90095

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3Division of Endocrinology, Diabetes and Metabolism (L.N., S.R., S.W.), Burns and Allen Research Center, Cedars-Sinai Medical Center, David Geffen School of Medicine, Los Angeles, California 90048

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3Division of Endocrinology, Diabetes and Metabolism (L.N., S.R., S.W.), Burns and Allen Research Center, Cedars-Sinai Medical Center, David Geffen School of Medicine, Los Angeles, California 90048

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4Medical University of South Carolina (B.H.), Charleston, South Carolina 29425

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5Department of Biochemistry (H.F.D.), The University of Wisconsin, Madison, Wisconsin 53706

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1Department of Orthopaedic Surgery (N.L., R.F.C., V.L., J.S.A., M.H.), UCLA, Los Angeles, California 90095

2David Geffen School of Medicine, and Molecular Biology Institute (J.S.A., M.H.), UCLA, Los Angeles, California 90095

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1Department of Orthopaedic Surgery (N.L., R.F.C., V.L., J.S.A., M.H.), UCLA, Los Angeles, California 90095

2David Geffen School of Medicine, and Molecular Biology Institute (J.S.A., M.H.), UCLA, Los Angeles, California 90095

*Address all correspondence and requests for reprints to: Martin Hewison, Ph.D., Department of Orthopaedic Surgery, David Geffen School of Medicine UCLA, 615 Charles E. Young Drive South, Los Angeles, California 90095.

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Received:

14 January 2008

Published:

01 October 2008

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Nancy Liu, Lisa Nguyen, Rene F. Chun, Venu Lagishetty, Songyang Ren, Shaoxing Wu, Bruce Hollis, Hector F. DeLuca, John S. Adams, Martin Hewison, Altered Endocrine and Autocrine Metabolism of Vitamin D in a Mouse Model of Gastrointestinal Inflammation, Endocrinology, Volume 149, Issue 10, 1 October 2008, Pages 4799–4808, https://doi.org/10.1210/en.2008-0060
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The active form of vitamin D, 1,25-dihydroxyvitamin D3, [1,25(OH)2D3] has potent actions on innate and adaptive immunity. Although endocrine synthesis of 1,25(OH)2D3 takes place in the kidney, the enzyme that catalyzes this, 25-hydroxyvitamin D-1α-hydroxylase (CYP27b1 in humans, Cyp27b1 in mice), is expressed at many extra-renal sites including the colon. We have shown previously that colonic expression of CYP27b1 may act to protect against the onset of colitis. To investigate this further, we firstly characterized changes in Cyp27b1 expression in a mouse model of colitis. Mice treated with dextran sodium sulfate (DSS) showed weight loss, histological evidence of colitis, and increased expression of inflammatory cytokines. This was associated with decreased renal expression of Cyp27b1 (5-fold, P = 0.013) and lower serum 1,25(OH)2D3 (51.8 ± 5.9 pg/nl vs. 65.1 ± 1.6 in controls, P < 0.001). However, expression of CYP27b1 was increased in the proximal colon of DSS mice (4-fold compared with controls, P < 0.001). Further studies were carried out using Cyp27b1 null (−/−) mice. Compared with +/− controls the Cyp27b1 −/− mice showed increased weight loss (4.9% vs. 22.8%, P < 0.001) and colitis. This was associated with raised IL-1 in the distal colon and IL-17 in the proximal and distal colon. Conversely, DSS-treated Cyp27b1−/− mice exhibited lower IL-10 in the proximal colon and toll-like receptors 2 and 4 in the distal colon. These data indicate that both local and endocrine synthesis of 1,25(OH)2D3 affect colitis in DSS-treated mice. Lack of Cyp27b1 exacerbates disease in this model, suggesting that similar effects may occur with vitamin D deficiency.

Copyright © 2008 by the Endocrine Society

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