Role of IGFBP7 in H1N1 influenza virus-induced inflammation and apoptosis in lung epithelial cells and related mechanism

Objective To investigate the role of insulin-like growth factor-binding protein 7 (IGFBP7) in H1N1 influenza virus-induced inflammation and apoptosis in lung epithelial cells and related mechanism.Methods The effect of H1N1 virus on IGFBP7 expression in A549 cells was detected by Western blot. The viability of lung epithelial A549 cells was assessed by MTT assay. The levels of inflammatory factors were examined by ELISA kits. The expression of apoptosis-associated protein cleaved-caspase-3 was measured by Western blot.Results H1N1 virus significantly inhibited the viability of A549 cells in a dose-time dependent manner (P<0.05). H1N1 virus markedly promoted IGFBP7 expression in a dose-time dependent manner (P<0.05). Interfering IGFBP7 dramatically reduced the levels of H1N1-induced inflammatory factors in A549 cells (P<0.05). Interfering IGFBP7 remarkably inhibited the phosphorylation of extracellular regulated protein kinase (ERK) and p65 (P<0.05). Overexpression of ERK or nuclear factor κB (NF-κB) significantly reversed the effect of IGFBP7 on inflammation and apoptosis in A549 cells (P<0.05).Conclusions Interfering IGFBP7 attenuates H1N1-induced inflammatory response and apoptosis in A549 cells through regulating the ERK/NF-κB signaling pathway, which provides a new idea for the treatment of influenza A virus-induced lung injury.