Department of Hematology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
The Jiangxi Province Key Laboratory of Hematologic Diseases, Nanchang, China.
Turk J Med Sci. 2024 Apr 15;54(5):1165-1174. doi: 10.55730/1300-0144.5895. eCollection 2024.
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.
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.
Vitamin D has potential as a supplementary treatment for NEC patients.
背景/目的：坏死性小肠结肠炎（NEC）是一种主要影响早产儿的严重疾病，涉及异常的免疫反应和炎症细胞因子释放，导致肠上皮损伤。本研究旨在探讨维生素 D 对 NEC 新生大鼠模型中树突状细胞（DC）成熟和激活的免疫调节作用及其对肠道的抗炎作用。
通过免疫组织化学染色、实时定量 PCR 和免疫荧光法评估肠道组织的炎症损伤，以及共刺激分子、炎症因子和免疫调节因子的 DC 表达和凋亡情况。通过异硫氰酸荧光素-卵清蛋白（FITC-OVA）摄取试验分析 DC 的内吞作用。
维生素 D 给药可减轻肠道损伤和凋亡，抑制 CD86 并增加 CD80 表达。体外脂多糖（LPS）刺激的 DC2.4 细胞中，CD86、肿瘤坏死因子-α（TNF-α）、白细胞介素 1β（IL-1β）、诱导型一氧化氮合酶（iNOS）和吲哚胺 2,3-双加氧酶 1（IDO-1）表达上调，除 IDO-1 外，这些表达均被维生素 D 下调。LPS 抑制 CD80 表达，而维生素 D 处理可恢复其表达，并改善内吞能力。维生素 D 可改善 NEC 新生大鼠的肠道损伤，并对 DC 发挥抗炎和免疫调节作用。
维生素 D 可能成为 NEC 患者的辅助治疗药物。
