TLR and NLRs Signaling May Synergistically Affect Expression of IRFs in Mouse Pleuropneumonia Model Induced by <i>Actinobacillus pleuropneumoniae</i>

Abstract

Porcine contagious pleuropneumonia, caused by <i>Actinobacillus pleuropneumoniae </i>(App), is a very important disease in pig industry. NLRs and TLRs may involve in the pathogenesis of this disease. It was reported that IRFs played an important role in regulating the expression of inflammatory factors during infectious diseases, thus regulating the occurrence of inflammation and the antibacterial reaction, In order to investigate their role in the pathogenesis of pulmonary lesions in porcine contagious pleuropneumonia, we employed a mouse model of intranasal infection by App, which resulted in lung inflammation. Mice showed dyspnea and anorexia after intranasal inoculation with App at post-inoculation 48 h. In the autopsy, the lungs were found to be severely damaged by acute hemorrhagic pneumonia. The histopathologic changes were characterized by hemorrhage, eosnophils and lymphocyte infiltration. Expression of interleukin-8 (IL-8), IL-10, IL-1β、IL-6, interferon-α(INF-α), toll-like receptor-2 (TLR-2), TLR-4, interferon regulatory factor-1(IRF-1), IRF-5, IRF-7, and NLRP-3 were increased significantly concomitantly with decreased expression of IRF-3 and IRF-4 in the lung of App infected mice compared with control (<I>P<0.05</I> or <I>P<0.01</I>). The present results suggest that TLR/NLRs signaling may synergistically activate IRFs in mouse pleuropneumonia model induced by App and then regulate the inflammatory response and lung inflammation in mice.