Vitamin D, immune regulation, the microbiota, and inflammatory bowel disease

被引：105

作者：

Cantorna, Margherita T. ^{[1
,2
]}

McDaniel, Kaitlin ^{[1
]}

Bora, Stephanie ^{[1
]}

Chen, Jing ^{[1
]}

James, Jamaal ^{[1
]}

机构：

[1] Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA

[2] Penn State Univ, Ctr Mol Immunol & Infect Dis, University Pk, PA 16802 USA

来源：

EXPERIMENTAL BIOLOGY AND MEDICINE | 2014年 / 239卷 / 11期

基金：

美国国家卫生研究院;

关键词：

Vitamin D; inflammatory bowel disease; microbiota; SULFATE-INDUCED COLITIS; D-RECEPTOR; CROHNS-DISEASE; ULCERATIVE-COLITIS; T-CELLS; 1,25-DIHYDROXYVITAMIN D-3; ENTERIC MICROFLORA; MICE; PATHOGENESIS; GENE;

D O I：

10.1177/1535370214523890

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The inflammatory bowel diseases are complex diseases caused by environmental, immunological, and genetic factors. Vitamin D status is low in patients with inflammatory bowel diseases, and experimental inflammatory bowel diseases are more severe in vitamin D-deficient or vitamin D receptor knockout animals. Vitamin D is beneficial in inflammatory bowel diseases because it regulates multiple checkpoints and processes essential for homeostasis in the gut. Vitamin D inhibits IFN-gamma and IL-17 production while inducing regulatory T cells. In addition, vitamin D regulates epithelial cell integrity, innate immune responses, and the composition of the gut microbiota. Overall, vitamin D regulates multiple pathways that maintain gastrointestinal homeostasis. The data support improving vitamin D status in patients with inflammatory bowel diseases.

引用

页码：1524 / 1530

页数：7

共 73 条

[1] Higher Predicted Vitamin D Status Is Associated With Reduced Risk of Crohn's Disease [J].

Ananthakrishnan, Ashwin N. ;

Khalili, Hamed ;

Higuchi, Leslie M. ;

Bao, Ying ;

Korzenik, Joshua R. ;

Giovannucci, Edward L. ;

Richter, James M. ;

Fuchs, Charles S. ;

Chan, Andrew T. .

GASTROENTEROLOGY, 2012, 142 (03) :482-489

[2]

Molodecky Natalie A, 2010, Gastroenterol Hepatol (N Y), V6, P339

[3] Host-bacterial mutualism in the human intestine [J].

Bäckhed, F ;

Ley, RE ;

Sonnenburg, JL ;

Peterson, DA ;

Gordon, JI .

SCIENCE, 2005, 307 (5717) :1915-1920

[4] The biology of NKT cells [J].

Bendelac, Albert ;

Savage, Paul B. ;

Teyton, Luc .

ANNUAL REVIEW OF IMMUNOLOGY, 2007, 25 :297-336

[5] Vitamin D Deficiency Is Associated with Ulcerative Colitis Disease Activity [J].

Blanck, Stacey ;

Aberra, Faten .

DIGESTIVE DISEASES AND SCIENCES, 2013, 58 (06) :1698-1702

[6] Converging pathways lead to overproduction of IL-17 in the absence of vitamin D signaling [J].

Bruce, Danny ;

Yu, Sanhong ;

Ooi, Jot Hui ;

Cantorna, Margherita T. .

INTERNATIONAL IMMUNOLOGY, 2011, 23 (08) :519-528

[7] Intrinsic Requirement for the Vitamin D Receptor in the Development of CD8αα-Expressing T Cells [J].

Bruce, Danny ;

Cantorna, Margherita T. .

JOURNAL OF IMMUNOLOGY, 2011, 186 (05) :2819-2825

[8] Disruption of a new forkhead/winged-helix protein, scurfin, results in the fatal lymphoproliferative disorder of the scurfy mouse [J].

Brunkow, ME ;

Jeffery, EW ;

Hjerrild, KA ;

Paeper, B ;

Clark, LB ;

Yasayko, SA ;

Wilkinson, JE ;

Galas, D ;

Ziegler, SF ;

Ramsdell, F .

NATURE GENETICS, 2001, 27 (01) :68-73

[9] Vitamin D, multiple sclerosis and inflammatory bowel disease [J].

Cantorna, Margherita T. .

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2012, 523 (01) :103-106

[10] Why do T cells express the vitamin D receptor? [J].

Cantorna, Margherita T. .

YEAR IN IMMUNOLOGY, 2011, 1217 :77-82

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