Protective effects of vitamin D against injury in intestinal epithelium
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Read the article on link.springer.com ↗Article · Oct 2019 · 1 min read
In brief
In brief
This preclinical study demonstrates that vitamin D protects intestinal epithelial cells from LPS-induced injury by restoring tight junction proteins (ZO-1, claudin-2), reducing permeability, and decreasing inflammatory cytokines. Using both cell culture and organoid models, the research supports vitamin D supplementation as a potential therapeutic strategy for preventing acute intestinal injury in at-risk infants.
Written by the GCMD Library team from the article.
Abstract
Background
Vitamin D deficiency is associated with intestinal barrier dysfunction, which contributes to pathogenesis of acute intestinal injury in children. We aim to investigate the effects of vitamin D on intestinal injury in intestinal epithelial cells and organoids.
Methods
Lipopolysaccharide (LPS) was used to induce injury in intestinal epithelial cells (IEC-18) and organoids, and the effect of vitamin D was assessed. Cell viability was measured and inflammation cytokines TNFα and IL-8 were quantified. FITC-dextran 4 kDa (FD4) permeability was measured using Transwell while tight junction markers were assessed by immunofluorescence staining in IEC-18 and intestinal organoids. Data were compared using one-way ANOVA with Bonferroni post-test.
Results
IEC-18 viability was decreased by LPS treatment, but was prevented by vitamin D. The upregulation of inflammation was inhibited by vitamin D, which also decreased epithelium permeability. Vitamin D restored tight junction ZO-1 and claudin 2. In addition, vitamin D decreased TNFα expression and prevented the disruption of ZO-1 in injured organoids.
Conclusions
Vitamin D rescued epithelial barrier function by improving permeability and restoring tight junctions, leading to decrease inflammation. This study confirms the protective effects of vitamin D, which could be used as a treatment strategy for infants at risk of developing intestinal injury.