IFN-τ Alleviates Lipopolysaccharide-Induced Inflammation by Suppressing NF-κB and MAPKs Pathway Activation in Mice

IFN-tau, which is a type I interferon with low cytotoxicity, is defined as a pregnancy recognition signal in ruminants. Type I interferons have been used as anti-inflammatory agents, but their side effects limit their clinical application. The present study aimed to determine the anti-inflammatory effects of IFN-tau in a lipopolysaccharide-stimulated acute lung injury (ALI) model and in RAW264.7 cells and to confirm the mechanism of action involved. The methods used included histopathology, measuring the lung wet/dry ratio, determining the myeloperoxidase activity, ELISA, qPCR, and western blot. The results revealed that IFN-tau greatly ameliorated the infiltration of inflammatory cells and the expression of TNF-alpha, IL-1 beta, and IL-6. Further analysis revealed that IFN-tau down-regulated the expression of TLR-2 and TLR-4 mRNA and the activity of the NF-kappa B and MAPK pathways both in a lipopolysaccharide-induced ALI model and in RAW264.7 cells. The results demonstrated that IFN-tau suppressed the levels of pro-inflammatory cytokines by inhibiting the phosphorylation of the NF-kappa B and MAPK pathways. Thus, IFN-tau may be an optimal target for the treatment of inflammatory diseases.