Study On IL-17-mediated Pulmonary Inflammatory Response In A Mouse Model Of Contagious Caprine Pleuropneumoniae

Contagious caprine pleuropneumoniae(CCPP)is a highly contagious disease caused by Mycoplasma capricolum subsp.capripneumoniae(Mccp).The prevalence of CCPP poses a serious threat to goat farming worldwide.At present,the research on CCPP is mostly focused on the isolation and identification of pathogens and epidemiological investigations.There are few reports on the mechanism of immune pathogenesis of this disease.This is mainly limited by the fact that there are too few types of goat immunoassay reagents.Therefore,establishing a CCPP mouse model is of great significance for studying the immune response mechanism after Mccp infection.Based on this,F38 standard strain was used as the material,and BABL/c mice were used as the experimental animals in this study.Mccp-induced CCPP mouse model was constructed by intranasal inoculation,thoracic inoculation,direct intraperitoneal inoculation and intraperitoneal inoculation after antibiotic pretreatment.Mouse models were identified by H.E staining,histopathological scoring and Mccp real-time PCR.Real-time PCR was used to detect IL-17-related cytokines,chemokines and receptor mRNA levels in lung tissue.The content of IL-17 was detected by ELISA in serum and lung homogenate supernatant,and the number of neutrophils and macrophages in lung tissue was detected by flow cytometry.The present study explored that the involvement of IL-17 in Mccp-induced pulmonary inflammatory response in a mouse model of CCPP.The study obtained the following results:1.A mouse model of CCPP was established.After 400μL of 3.252×10~8 copies of PBS resuspended F38 bacteria were injected into mice by intraperitoneal inoculation,the lungs showed“liver-like changes”,severe hemorrhage,thickened alveolar wall,local alveolar dilation,and incomplete lung tissue structure.And there was inflammatory cell infiltration in the lung tissue.The Mccp load in the lungs of the experimental group was 5.9×10~4 copies/μL,which was significantly different from the control group(P<0.001);2.The IL-17 mRNA level in lung tissue of CCPP model mice was significantly increased,and the mRNA levels of IL-17-related cytokines,such as IL-1β,IL-6 and IL-27,were prominently increased;And chemokines in lung tissues(CXCL1,CXCL2),CXCL5)and chemokine ligands(CCL20,CCL2)mRNA levels were also markedly increased;The results of ELISA showed that the content of IL-17 in serum and lung tissue was remarkably increased;3.The results of flow cytometry showed that the number of neutrophils and macrophages in lung tissue of CCPP model mice were noticeable increased.In conclusion:1.A mouse model of CCPP was established,successfully;2.IL-17 mediates pulmonary inflammation in a CCPP mouse model by chemotaxis of inflammatory cells such as neutrophils.