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Intestinal Epithelial Regeneration in Response to Ionizing Irradiation
Published on: July 27, 2022
Protective effects of vitamin D against injury in intestinal epithelium
Carol Lee1, Ethan Lau1, Sinobol Chusilp1,2
1Division of General and Thoracic Surgery, Translational Medicine Program, Hospital for Sick Children, University of Toronto, 1526-555 University Ave, Toronto, ON, M5G 1X8, Canada.
Insights
Vitamin D protects against intestinal injury by improving gut barrier function and reducing inflammation. This finding suggests vitamin D as a potential treatment for infants at risk of acute intestinal injury.
Area of Science:
- Gastroenterology
- Pediatric Medicine
- Cell Biology
Background:
- Vitamin D deficiency is linked to intestinal barrier dysfunction and acute intestinal injury in children.
- Investigating vitamin D's role in protecting intestinal epithelial cells and organoids is crucial.
Purpose of the Study:
- To determine the protective effects of vitamin D on intestinal epithelial cells and organoids against injury.
- To assess vitamin D's impact on intestinal barrier function, inflammation, and cell viability.
Main Methods:
- Lipopolysaccharide (LPS) induced injury in intestinal epithelial cells (IEC-18) and organoids.
- Assessed cell viability, quantified inflammatory cytokines (TNF-α, IL-8), and measured epithelial permeability using FITC-dextran.
- Evaluated tight junction markers (ZO-1, claudin 2) via immunofluorescence.
Main Results:
- Vitamin D prevented LPS-induced decrease in cell viability and reduced inflammation.
- Vitamin D treatment decreased epithelial permeability and restored tight junction proteins (ZO-1, claudin 2).
- In organoids, vitamin D reduced TNF-α expression and preserved ZO-1 integrity.
Conclusions:
- Vitamin D enhances epithelial barrier function by improving permeability and restoring tight junctions, thereby reducing inflammation.
- These findings support vitamin D's protective role against intestinal injury.
- Vitamin D presents a potential therapeutic strategy for infants susceptible to intestinal injury.
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.
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