The intestinal vitamin D receptor in inflammatory bowel disease: inverse correlation with inflammation but no relationship with circulating vitamin D status.
Crohn’s disease
inflammatory bowel disease
ulcerative colitis
vitamin D
vitamin D receptor
Journal
Therapeutic advances in gastroenterology
ISSN: 1756-283X
Titre abrégé: Therap Adv Gastroenterol
Pays: England
ID NLM: 101478893
Informations de publication
Date de publication:
2019
2019
Historique:
received:
31
08
2018
accepted:
28
11
2018
entrez:
6
2
2019
pubmed:
6
2
2019
medline:
6
2
2019
Statut:
epublish
Résumé
The intestinal vitamin D receptor (VDR) remains poorly characterized in patients with inflammatory bowel disease (IBD). Colonoscopic biopsies and intestinal resection specimens from the terminal ileum, ascending and sigmoid colon, from patients with and without IBD, were analyzed for VDR mRNA quantification by polymerase chain reaction, and protein localization and semi-quantification by immunohistochemistry. The relationship between VDR and intestinal inflammation, serum 25(OH)D and oral vitamin D intake was elicited. A total of 725 biopsies from 20 patients with Crohn's disease (CD), 15 with ulcerative colitis (UC) and 14 non-IBD controls who underwent colonoscopy were studied. VDR gene expression and protein staining intensity was similar across all three groups, and across the intestinal segments. Sigmoid colon VDR mRNA expression inversely correlated with faecal calprotectin ( VDR transcript expression and protein staining intensity are inversely related to inflammation in IBD, but unrelated to serum 25(OH)D, and similar to non-IBD controls. Strategies to upregulate intestinal VDR, potentially translating to modulation of disease activity, require investigation.
Sections du résumé
BACKGROUND
BACKGROUND
The intestinal vitamin D receptor (VDR) remains poorly characterized in patients with inflammatory bowel disease (IBD).
METHODS
METHODS
Colonoscopic biopsies and intestinal resection specimens from the terminal ileum, ascending and sigmoid colon, from patients with and without IBD, were analyzed for VDR mRNA quantification by polymerase chain reaction, and protein localization and semi-quantification by immunohistochemistry. The relationship between VDR and intestinal inflammation, serum 25(OH)D and oral vitamin D intake was elicited.
RESULTS
RESULTS
A total of 725 biopsies from 20 patients with Crohn's disease (CD), 15 with ulcerative colitis (UC) and 14 non-IBD controls who underwent colonoscopy were studied. VDR gene expression and protein staining intensity was similar across all three groups, and across the intestinal segments. Sigmoid colon VDR mRNA expression inversely correlated with faecal calprotectin (
CONCLUSIONS
CONCLUSIONS
VDR transcript expression and protein staining intensity are inversely related to inflammation in IBD, but unrelated to serum 25(OH)D, and similar to non-IBD controls. Strategies to upregulate intestinal VDR, potentially translating to modulation of disease activity, require investigation.
Identifiants
pubmed: 30719077
doi: 10.1177/1756284818822566
pii: 10.1177_1756284818822566
pmc: PMC6348511
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1756284818822566Déclaration de conflit d'intérêts
Conflict of interest statement: The authors declare that there is no conflict of interest.
Références
J Immunol. 2000 Mar 1;164(5):2405-11
pubmed: 10679076
Gut. 2000 Aug;47(2):211-4
pubmed: 10896912
Gut. 2000 Sep;47(3):404-9
pubmed: 10940279
Gut. 2006 Jun;55(6):749-53
pubmed: 16698746
Endocrinology. 2006 Dec;147(12):5542-8
pubmed: 16946007
J Cell Biochem. 2007 Apr 15;100(6):1395-405
pubmed: 17115413
J Pharmacol Exp Ther. 2008 Jan;324(1):23-33
pubmed: 17911375
Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G208-16
pubmed: 17962355
Mol Aspects Med. 2008 Dec;29(6):407-14
pubmed: 18727936
J Immunol. 2009 Feb 15;182(4):2074-83
pubmed: 19201860
Inflamm Bowel Dis. 2009 Nov;15(11):1656-62
pubmed: 19408329
Cell Host Microbe. 2009 Sep 17;6(3):231-43
pubmed: 19748465
J Immunol. 2009 Nov 1;183(9):5458-67
pubmed: 19843932
Aliment Pharmacol Ther. 2010 Aug;32(3):377-83
pubmed: 20491740
Endocrinol Metab Clin North Am. 2010 Jun;39(2):255-69, table of contents
pubmed: 20511050
Am J Pathol. 2010 Aug;177(2):686-97
pubmed: 20566739
Nat Rev Drug Discov. 2010 Dec;9(12):941-55
pubmed: 21119732
Mol Cell Endocrinol. 2011 Dec 5;347(1-2):11-6
pubmed: 21664245
J Immunol. 2012 Mar 1;188(5):2127-35
pubmed: 22301548
Aliment Pharmacol Ther. 2012 Aug;36(4):324-44
pubmed: 22686333
Nephron Exp Nephrol. 2012;122(1-2):36-50
pubmed: 23548800
Clin Transl Gastroenterol. 2013 Apr 18;4:e33
pubmed: 23594800
J Clin Invest. 2013 Sep;123(9):3983-96
pubmed: 23945234
Inflamm Bowel Dis. 2013 Nov;19(12):2634-43
pubmed: 24105392
Gut. 2015 Jul;64(7):1082-94
pubmed: 25080448
Dig Dis Sci. 2015 Aug;60(8):2427-35
pubmed: 25757449
Cancer Prev Res (Phila). 2015 May;8(5):387-99
pubmed: 25873367
United European Gastroenterol J. 2015 Jun;3(3):294-302
pubmed: 26137304
World J Gastroenterol. 2016 Apr 7;22(13):3581-91
pubmed: 27053850
Clin Gastroenterol Hepatol. 2017 Feb;15(2):240-246.e1
pubmed: 27266980
Am J Clin Nutr. 2016 Jul;104(1):113-20
pubmed: 27281309
Front Physiol. 2016 Nov 15;7:498
pubmed: 27895587
Dig Dis Sci. 2017 Feb;62(2):448-455
pubmed: 27975236
Immunology. 1987 Aug;61(4):457-61
pubmed: 2832307
Clin Nutr. 2018 Aug;37(4):1375-1382
pubmed: 28651829
Innate Immun. 2017 Aug;23(6):557-565
pubmed: 28770666
Endocrinology. 2018 Feb 1;159(2):967-979
pubmed: 29228157
J Crohns Colitis. 2018 Jul 30;12(8):963-972
pubmed: 29726893
Inflamm Bowel Dis. 2018 Jun 8;24(7):1462-1470
pubmed: 29788141
J Clin Endocrinol Metab. 2018 Sep 1;103(9):3267-3277
pubmed: 29947775
J Control Release. 2018 Sep 28;286:94-102
pubmed: 30017723
Sci Rep. 2018 Jul 31;8(1):11511
pubmed: 30065252
Gastroenterology. 1998 Feb;114(2):262-7
pubmed: 9453485