High Expression of Bpifb1 Stimulates Macrophages to Secrete Inflammatory Factors and inducing Pulmonary Fibrosis

High Expression of Bpifb1 Stimulates Macrophages to Secrete Inflammatory Factors and inducing Pulmonary Fibrosis <bold>Background:</bold> Pulmonary fibrosis is a chronic and progressive lung disease, leading to severe impairments in respiratory function. Macrophages play a pivotal role in the pathogenesis of pulmonary fibrosis, largely through the secretion of pro-inflammatory and pro-fibrotic factors. Bpifb1 is a protein known for its involvement in innate immune responses. <bold>Objective:</bold> This study aims to investigate the effect of Bpifb1 overexpression in macrophages on the secretion of inflammatory factors and its subsequent role in the induction and progression of pulmonary fibrosis. <bold>Methods:</bold> We utilized both in vitro and in vivo models to explore the impact of Bpifb1 overexpression. In vitro, macrophages were genetically modified to overexpress Bpifb1, and the secretion levels of inflammatory cytokines were measured using ELISA. In vivo, a mouse model of pulmonary fibrosis was employed, wherein Bpifb1 overexpression was achieved through adenoviral vectors. Pulmonary fibrosis were assessed via histological analyses and lung function tests. <bold>Results:</bold> Our findings demonstrate that overexpression of Bpifb1 in macrophages significantly increases the secretion of key inflammatory cytokines, including TNF-alpha and IL-6. In vivo studies further revealed that mice with Bpifb1 overexpression exhibited accelerated progression of pulmonary fibrosis, characterized by increased lung collagen deposition and impaired lung function, compared to control mice. <bold>Conclusion:</bold> Bpifb1 as a potential therapeutic target in the treatment and management of pulmonary fibrosis-mediated inflammation and fibrosis.