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Abstract <p>The lungs are an important target for vitamin D ((VitD)). Poor vitamin D status is associated with bronchopulmonary dysplasia. Our aim is to investigate the effect of Vitamin D on the biological changes of bronchial associated cells induced by M1 macrophages using cell co-culture technique. M0 macrophages induced by LPS and IFN-γ were pretreated with VitD, and then co-cultured with alveolar type 2 epithelial (AT 2) cells, pulmonary fibroblasts (PF), and pulmonary vascular endothelial cells (PVEC). The cells were&#xa0;divided into control group, macrophage co-culture group, and VitD pretreatment group. Then followed CCK8, western blot, flow cytometry and EdU assay. Cell proliferation was inhibited, the protein expression&#xa0;levels of E-cad and SPC in AT 2 cells decreased, and the expression levels of N-cad and α-SMA increased. Pretreatment with VitD can significantly increase the levels of E-cad and SPC, and decrease the levels of N-cad and α-SMA. Cell co-culture significantly promoted apoptosis, and inhibited migration of PVECs, while pretreatment with VitD significantly inhibited apoptosis and promoted cell migration of PVECs. In addition, cell co-culture significantly inhibited the expression of PCNA, Collagen I, and Collagen III in PFs, while VitD pretreatment significantly promoted the expression of PCNA, Collagen I, and Collagen III. Therefore, in inflammatory environment, VitD could inhibit the epithelial-mesenchymal transition (EMT) process of AT 2 cells, restore the proliferation and migration of vascular endothelial cells, and promote the proliferation of lung fibroblasts, thus may be beneficial for the treatment of lung injury in preterm infants with bronchial dysplasia.</p>

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Vitamin D Exerts Anti-Inflammatory Effects by M1 Macrophages in an Inflammatory Environment of Lung Cells

  • 期刊论文

  • 发表日期：

    2026年7月9日

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  • H. Zhen,
  • Q. Wei,
  • B. Wei,
  • M. Liang,
  • Q. Huang,
  • R. Li

摘要

Abstract

The lungs are an important target for vitamin D ((VitD)). Poor vitamin D status is associated with bronchopulmonary dysplasia. Our aim is to investigate the effect of Vitamin D on the biological changes of bronchial associated cells induced by M1 macrophages using cell co-culture technique. M0 macrophages induced by LPS and IFN-γ were pretreated with VitD, and then co-cultured with alveolar type 2 epithelial (AT 2) cells, pulmonary fibroblasts (PF), and pulmonary vascular endothelial cells (PVEC). The cells were divided into control group, macrophage co-culture group, and VitD pretreatment group. Then followed CCK8, western blot, flow cytometry and EdU assay. Cell proliferation was inhibited, the protein expression levels of E-cad and SPC in AT 2 cells decreased, and the expression levels of N-cad and α-SMA increased. Pretreatment with VitD can significantly increase the levels of E-cad and SPC, and decrease the levels of N-cad and α-SMA. Cell co-culture significantly promoted apoptosis, and inhibited migration of PVECs, while pretreatment with VitD significantly inhibited apoptosis and promoted cell migration of PVECs. In addition, cell co-culture significantly inhibited the expression of PCNA, Collagen I, and Collagen III in PFs, while VitD pretreatment significantly promoted the expression of PCNA, Collagen I, and Collagen III. Therefore, in inflammatory environment, VitD could inhibit the epithelial-mesenchymal transition (EMT) process of AT 2 cells, restore the proliferation and migration of vascular endothelial cells, and promote the proliferation of lung fibroblasts, thus may be beneficial for the treatment of lung injury in preterm infants with bronchial dysplasia.