The Expression of VDBP in the Severe COVID-19 and its Role in Acute Lung Injury

Abstract

Abstract Background Vitamin D-binding protein (VDBP) may be involved in the occurrence and development of COVID-19. This study intends to investigate the expression of VDBP in COVID-19 and to explore the role of VDBP through animal and cellular models of acute lung injury (ALI). Methods The serum of COVID-19 and common pneumonia over 65 years old in the Department of Geriatrics of the Shandong Provincial Hospital Affiliated to Shandong First Medical University were collected from 1 December 2022 to 30 July 2023. ELISA was used to detect the expression of serum VDBP. The mouse model of ALI was established by intraperitoneal injection of LPS, and the expression of VDBP in the lung tissue of ALI mice was detected by immunohistochemistry and Western blot. Construct a VDBP gene-silencing plasmid and transfect it into human alveolar epithelial A549 cells. After 72 hours of LPS intervention, collect cells and cell supernatant for testing. CCK8 detection of cell proliferation. Flow cytometry was used to detect apoptosis in cells. Results The VDBP of severe COVID-19 was higher than that of non-severe COVID-19 and common pneumonia (p < 0.05), but the VDBP was not an independent risk factor for the severity of COVID-19 (p > 0.05). Immunohistochemistry and Western blot suggest that VDBP in lung tissue of ALI mice was significant overexpression (p < 0.05). VDBP in LPS-induced injury of alveolar epithelial cells was significant overexpression (p < 0.05). The ELISA results showed that after LPS intervention, the inflammatory factor IL-1β and TNF-a was significantly reduced in the VDBP gene silencing group compared to the control group (p < 0.05). The cell proliferation ability of the VDBP gene silencing group was significantly increased compared to the control group, and the cell apoptosis rate was significantly reduced compared to the control group (p < 0.05). Conclusion The level of VDBP in severe COVID-19 was significantly increased. VDBP may play an inflammatory factor in ALI and promote apoptosis of bronchial epithelial cells.