Authors

Qing He1, #, Yi Yang2, 3, Pinglin Zhang4, Lijun Su4, Xinghui Zheng4, *


Departments

1Department of Neonatology, Affiliated Hospital of Guizhou Medical University, Guiyang 550000, Guizhou Province, China - 2Department of Children' s rehabilitation, The Third Affiliated Hospital of Zunyi Medical University/Zunyi First People's Hospital, Zunyi 563000, Guizhou Province, China - 3Department of Children's Rehabilitation, Zunyi First People's Hospital, Zunyi 563000, Guizhou Province, China - 4Department of Neonatology, The Third Affiliated Hospital of Zunyi Medical University/Zunyi First People's Hospital, Zunyi 563000, Guizhou Province, China

#These authors contributed equally to this work as co-first author

Abstract

Objective: To explore the mechanism by which vitamin D (VitD) inhibits the expression of surface molecules on lung dendritic cells (DCs) of young rats with sepsis to reduce the body's excessive inflammatory response. 

Methods: Healthy and clean male Sprague–Dawley pups were selected and the random number table method was used to divide all pups into a control group, a sepsis group, and a VitD intervention group. After establishing the sepsis model, blood was drawn from the young rats to test the serum 25(OH)D3 level; the lung tissue of the young rats was collected and the enzyme-linked immunosorbent assay (ELISA) was used to determine the serum interleukin-12 (IL-12) and tumor necrosis factor -α (TNF-α) level; flow cytometry was used to measure the expression rate of the DC surface molecules CD86 and CD83; HE staining was carried out and the pathological morphology of the lung tissue of each group of young rats was observed, and the infiltration of inflammatory cells was evaluated. 

Results: Compared with the control group, the 3-day survival rate, serum 25(OH)D3 level, serum IL-12 and TNF-α levels, and the lung surface DCs on young rats in the sepsis group and VitD intervention group were significantly reduced (P<0.05) The expression rates of molecular CD86 and CD83 were significantly increased (P<0.05); compared with the sepsis group, the 3-day survival rate, serum 25(OH)D3 levels of young rats in the VitD intervention group were significantly increased (P<0.05), and levels of serum IL-12 and TNF-α, and the expression rates of CD86 and CD83 on the surface of lung DCs were significantly reduced (P<0.05). The lung tissue and pathological structure of the control pups were normal, and there was no inflammatory cell infiltration in the lung interstitium; the lung tissues of the sepsis group pups showed swelling of alveolar epithelial cells, accompanied by congestion and pulmonary interstitial congestive edema, and a large amount of inflammatory cell infiltration: The degree of swelling of lung alveolar epithelial cells in the VitD intervention group was slightly lower in the sepsis group; the congestion and congestive edema were reduced, and there was a small amount of inflammatory cell infiltration. 

Conclusion: VitD can reduce the body’s excessive inflammatory response by inhibiting the expression of surface molecules of DCs in the lungs of young rats with sepsis.


Keywords

Sepsis, vitamin D, dendritic cells, inflammatory factors

DOI:

10.19193/0393-6384_2022_2_135