期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms22010362
关键词
antimicrobial peptides (AMP); Crohn's disease; dysbiosis; epigenetics; inflammation; metabolites; microbiome; micronutrient; nuclear receptor; probiotics; tight junctions; ulcerative colitis; vitamin D; VDR
资金
- Sao Paulo Research Foundation (FAPESP) [2018/21584-4, 2019/02583-0]
- FoRC-Food Research Center (FAPESP) [2013/07914-8]
- CAPES Foundation [88881.187323/2018-01, 88882.376972-2019-01, 88882.376365/2019-01]
- NIDDK/National Institutes of Health [R01 DK105118, R01DK114126]
- DOD CDMRP [BC191198]
- DOD [BC160450P1]
Inflammatory bowel disease is a chronic inflammation of the GI tract, including Crohn's disease and ulcerative colitis, associated with microbiota dysbiosis and vitamin D deficiency. Further studies are needed to explore the mechanisms and therapeutic potential related to vitamin D/VDR in gut microbiota modulation for IBD.
Inflammatory bowel disease (IBD) is a chronic inflammation of the gastrointestinal tract (GIT), including Crohn's disease (CD) and ulcerative colitis (UC), which differ in the location and lesion extensions. Both diseases are associated with microbiota dysbiosis, with a reduced population of butyrate-producing species, abnormal inflammatory response, and micronutrient deficiency (e.g., vitamin D hypovitaminosis). Vitamin D (VitD) is involved in immune cell differentiation, gut microbiota modulation, gene transcription, and barrier integrity. Vitamin D receptor (VDR) regulates the biological actions of the active VitD (1 alpha,25-dihydroxyvitamin D3), and is involved in the genetic, environmental, immune, and microbial aspects of IBD. VitD deficiency is correlated with disease activity and its administration targeting a concentration of 30 ng/mL may have the potential to reduce disease activity. Moreover, VDR regulates functions of T cells and Paneth cells and modulates release of antimicrobial peptides in gut microbiota-host interactions. Meanwhile, beneficial microbial metabolites, e.g., butyrate, upregulate the VDR signaling. In this review, we summarize the clinical progress and mechanism studies on VitD/VDR related to gut microbiota modulation in IBD. We also discuss epigenetics in IBD and the probiotic regulation of VDR. Furthermore, we discuss the existing challenges and future directions. There is a lack of well-designed clinical trials exploring the appropriate dose and the influence of gender, age, ethnicity, genetics, microbiome, and metabolic disorders in IBD subtypes. To move forward, we need well-designed therapeutic studies to examine whether enhanced vitamin D will restore functions of VDR and microbiome in inhibiting chronic inflammation.
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