2020
DOI: 10.1016/j.autrev.2020.102672
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Mucosal vitamin D signaling in inflammatory bowel disease

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Cited by 35 publications
(27 citation statements)
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“…Other factors that may contribute to the depletion of vitamin D in PLE patients include: ongoing systemic inflammation, reduced dietary intake of vitamin D and increased vitamin D metabolism. Additionally, 1,25(OH) 2 D has immunomodulatory effects which may support mucosal health (Kellermann et al 2020). Due to this immunomodulatory role, it is also possible that patients with PLE develop this disease in part due to their 25(OH)D deficiency (Ananthakrishnan 2016).…”
Section: Gastrointestinal Diseasesmentioning
confidence: 99%
“…Other factors that may contribute to the depletion of vitamin D in PLE patients include: ongoing systemic inflammation, reduced dietary intake of vitamin D and increased vitamin D metabolism. Additionally, 1,25(OH) 2 D has immunomodulatory effects which may support mucosal health (Kellermann et al 2020). Due to this immunomodulatory role, it is also possible that patients with PLE develop this disease in part due to their 25(OH)D deficiency (Ananthakrishnan 2016).…”
Section: Gastrointestinal Diseasesmentioning
confidence: 99%
“…It has been found that the induction of antimicrobial peptide genes’ expression by vitamin D [ 9 ] explores the ‘antibiotic’ effect of vitamin D. Increasing research projects have unraveled the important role of vitamin D in the regulation of innate and adaptive immunity [ 10 , 11 , 12 ]. 1,25-dihydroxyvitamin D3 (1,25D3), the active form of vitamin D, induced the expression of two AMPs, hBD-2 and cathelicidin [ 13 , 14 ], in several cultured cells in response to bacterial pathogens.…”
Section: Introductionmentioning
confidence: 99%
“…In view of the above, it is not surprising that dysregulation in these components, such as defective expression of defensins, upregulation of claudin-2, or increased apoptosis of epithelial cells, can contribute to the disruption of the mucosal barrier, as reported in IBD and SpA patients [34][35][36][37][38]. In particular, it has been hypothesized that, in SpA patients, the increased intestinal permeability, probably induced by genetic factors (HLA-B27), could induce a disruption of the basal membrane, hyperplasia of goblet cells, and activation of Paneth cells producing high levels of anti-microbial peptides (AMPs) and IL-23, leading to exaggerated antigenic stimulation and activation of effector T-cells of the intestinal mucosa [27,[39][40][41][42][43].…”
Section: Vitamin D and Intestinal Permeabilitymentioning
confidence: 99%
“…Deficits in the autophagy mechanism can alter Paneth cell function and contribute to gut inflammation and dysbiosis. Low levels of intestinal epithelial VDR correlate with a reduced expression of the autophagy gene ATG16L1 and impaired antimicrobial function of Paneth cells [47,60] and can induce gut dysbiosis in patients with IBD [34].…”
Section: Vitamin D Mucosal Immunity and Immunomodulationmentioning
confidence: 99%