Pathogenesis pathways of idiopathic pulmonary fibrosis in bleomycin-induced lung injury model in mice

• We used animal model to research the potential pathogenesis of BLM induced lung injury.
• Increasing levels of TGF-β1 lead to activated Smad3 bound to the IL-31 promoter region, and the activation of STAT1.
• The inhibitor of TGF-β1 receptor decreased the IL-31 expression.
• Knocking-down of IL-31 decreased the STAT1 expression.

Our objective was to investigate the pathogenesis pathways of idiopathic pulmonary fibrosis (IPF). Bleomycin (BLM) induced animal models of experimental lung fibrosis were used. CHIP assay was executed to find the link between Smad3 and IL-31, and the expressions of TGF-β1, Smad3, IL-31 and STAT1 were detected to find whether they were similar with each other. We found that in the early injury or inflammation of the animal model, BLM promoted the development of inflammation, leading to severe pulmonary fibrosis. Then the expression of TGF-β1 and Smad3 increased. Activated Smad3 bound to the IL-31 promoter region, followed by the activation of JAK-STAT pathways. The inhibitor of TGF-β1 receptor decreased the IL-31 expression and knocking-down of IL-31 also decreased the STAT1 expression. We conclude that there is a pathway of pathogenesis in BLM-induced mouse model that involves the TGF-β, IL-31 and JAKs/STATs pathway.