Vitamin D alleviates intestinal injury in necrotizing enterocolitis and lipopolysaccharide-induced inflammatory response in dendritic cells in rats.

BACKGROUND/AIM: Necrotizing enterocolitis (NEC) is a serious condition that predominantly affects premature infants and involves an aberrant immune response and inflammatory cytokine release resulting in intestinal epithelial damage. The current study investigated the immunoregulatory effects of vitamin D on the maturation and activation of dendritic cells (DCs) and the antiinflammatory impact on the intestines in a neonatal rat model of NEC.Materials and methods: Inflammatory damage to intestinal tissue was assessed via morphological changes and apoptosis and DC expression of costimulatory molecules, inflammatory factors, and immunoregulatory factors by immunohistochemical staining, quantitative real-time PCR, and immunofluorescence. The fluorescein isothiocyanate-ovalbumin (FITC-OVA) uptake assay was used to analyze DC endocytosis.

RESULTS

Vitamin D administration attenuated intestinal damage and apoptosis, inhibiting CD86 and increasing CD80 expression. Lipopolysaccharide (LPS)-challenged DC2.4 cells in vitro showed upregulated CD86, tumor necrosis factorα (TNF-α), interleukin1β (IL-1β), inducible nitric oxide synthase (iNOS), and indoleamine 2,3-dioxygenase 1 (IDO-1) expression, which were all reduced by vitamin D, except for IDO-1. LPS inhibited CD80 expression, which was restored by vitamin D treatment, and endocytic capacity was improved. Vitamin D ameliorated intestinal damage in neonatal rats with NEC and exerted antiinflammatory and immunomodulatory effects on DCs.

CONCLUSION

Vitamin D has potential as a supplementary treatment for NEC patients.