scholarly journals The Role of Vitamin D in the Pathogenesis of Inflammatory Bowel Disease

2019 ◽  
Vol 1 (1) ◽  
pp. 231-240 ◽  
Author(s):  
Stefano Nobile ◽  
Michela Tenace ◽  
Helen Pappa

Vitamin D has a complex role in the pathogenesis of inflammatory bowel disease (IBD), which is still under investigation. We conducted a literature search using PubMed through December 2018 through the use of relevant search terms. We found an abundance of evidence to support the role of vitamin D in regulating the innate and adaptive arms of the immune system. The pathogenesis of IBD implicates the immune dysregulation of these immune system components. Proof of concept of the vitamin’s role in the pathogenesis of IBD is the mapping of the vitamin D receptor in a region of chromosome 12, where IBD is also mapped, and specific VDR polymorphisms’ link to IBD phenotypes. Further research is needed to better delineate vitamin D’s role in preventing IBD and its potential as a therapeutic target for this disease.

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Phillips-Farfán Bryan ◽  
Carvajal Karla ◽  
Medina-Torres Edgar Alejandro ◽  
Espinosa-Padilla Sara Elva ◽  
Fabrias Gemma ◽  
...  

Inflammatory bowel disease (IBD) describes different illnesses characterized by chronic inflammation of the gastrointestinal tract. Although the pathogenic mechanisms leading to IBD are poorly understood, immune system disturbances likely underlie its development. Sphingolipids (SLs) have been identified as important players and promising therapeutic targets to control inflammation in IBD. Interestingly, it seems that microorganisms of the normal gut microbiota and probiotics are involved in sphingolipid function. However, there is a great need to investigate the role of SLs as intermediates in the crosstalk between intestinal immunity and microorganisms. This review focuses on recent investigations that describe some mechanisms involved in the regulation of cytokine profiles by SLs. We also describe the importance of gut microbiota in providing signaling molecules that favor the communication between resident bacteria and intestinal cells. This, in turn, modulates the immune response in the bowel and likely in other peripheral organs. The potential of SLs and gut microbiota as targets or therapeutic agents for IBD is also discussed.


2017 ◽  
Vol 16 (3) ◽  
pp. 347-353 ◽  
Author(s):  
Stephanie Bora ◽  
Margherita T. Cantorna

Vitamin D/UVR effects on T cells that are important in the development of inflammatory bowel disease (IBD).


2009 ◽  
Vol 48 (2) ◽  
pp. 142-151 ◽  
Author(s):  
Pieter PE van Lierop ◽  
Janneke N Samsom ◽  
Johanna C Escher ◽  
Edward ES Nieuwenhuis

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Marco Ardesia ◽  
Guido Ferlazzo ◽  
Walter Fries

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.


1992 ◽  
Vol 21 (2) ◽  
pp. 451-502
Author(s):  
Stefan Schreiber ◽  
Andreas Raedler ◽  
William F. Stenson ◽  
Richard P. MacDermott

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