Interleukin-35 reduces inflammation in acute lung injury through inhibiting TLR4/NF-κB signaling pathways

Acute lung injury (ALI) in children is a complex disease that is accompanied by an inflammatory response. The pathogenesis of ALI in children is not yet well understood. Mice with ALI exhibit inflammation of the lungs and decreased expression of interleukin (IL)-35. To investigate whether the function of IL-35 affects lipopolysaccharide (LPS)-induced ALI, IL-35 was overexpressed in cells. Enzyme-linked immunosorbent assays indicated decreased levels of IL-6 and tumor necrosis factor-α in LPS-induced and agomir-IL-35-treated murine RAW264.7 macrophages. Finally, toll-like receptor 4 (TLR4)/NF-κB signaling pathways were analyzed. The expression of TLR4, NF-κB p65 and NF-κB p50 were decreased, as was the degradation of NF-κB inhibitor-α, in LPS-induced and agomir-IL-35-treated murine RAW264.7 macrophages. The results of the present study demonstrated that IL-35 may exhibit a protective role in ALI by modulating the TLR4/NF-κB signaling pathways.