IL-27 attenuates the TGF-β1-induced proliferation, differentiation and collagen synthesis in lung fibroblasts

AimsPulmonary fibrosis is a type of chronic lung disease and has characteristics that progress quickly, has a high fatality rate and a poor therapeutic effect. Our previous research showed that interleukin-27(IL-27) potentially attenuates BLM-induced pulmonary fibrosis, but the function of IL-27 in lung fibroblasts (LFs) differentiation pulmonary fibrosis is yet to be known.Main methodsHere we investigated the effect of IL-27 on the proliferation, differentiation and collagen synthesis of lung fibroblasts induced by transforming growth factor-β1 (TGF-β1)using MTT, bromodeoxyuridine(BrdU) staining, real-time quantitative PCR(qPCR), Western blot, cell cycle FACS assay and immunofluorescence. We also examined the expression of the JAK/STAT and TGF-β1/Smad signaling pathway of IL-27 in lung fibroblasts.Key findingsTGF-β1 treated lung fibroblasts showed significantly increased proliferation, differentiation and collagen synthesis as well as overactivated JAK/STAT and TGF-β1/Smad signaling. However, the presence of IL-27 weakened these effects and obviously inactivated the JAK/STAT and TGF-β1/Smad signaling pathways.SignificanceOur results indicate that IL-27 may play an anti-fibrotic role in the development, differentiation and collagen synthesis in lung fibroblasts. These data also may provide a target gene therapy method in treating pulmonary fibrosis.