IFN-γ Mice Resist Actinobacillus pleuropneumoniae Infection by Promoting Early Lung IL-18 Release and PMN-I Accumulation.

Porcine pleuropneumonia is a common infectious disease of pigs caused by Interferon gamma (IFN-γ) expression increases in the lung of pigs after infection, but the role of IFN-γ during the infection is still obscure. In this study, an IFN-γ mouse infection model was established, and bacterial load, levels of inflammatory cytokines, and types of neutrophils in the lungs were studied at different times post- infection. We found that wild-type (WT) mice were more susceptible to than IFN-γ mice. At 6 h postinfection (hpi), the expression of interleukin 18 (IL-18) and IL-1β in the lungs of IFN-γ mice was significantly increased compared to WT mice. The bacterial load and levels of inflammatory cytokines (IL-1β and IL-6) of IFN-γ mice were significantly reduced at 12 hpi compared to WT mice. After an initial loss, the numbers of lung polymorphonuclear (PMN)-I cells dramatically increased in the lungs of IFN-γ but not WT mice, whereas PMN-II cells continually decreased. Finally, administration of IL-18 significantly reduced clinical scores and bacterial load in the lungs of -infected mice. This study identifies IFN-γ as a target for regulating the inflammatory response in the lung and provides a basis for understanding the course of clinical bacterial pneumonia and for the formulation of treatment protocols.