绵羊传染性胸膜肺炎，是由绵羊肺炎支原体引起的高度接触性传染病。有关绵羊肺炎支原体致病机制的研究相对滞后，尤其是其与宿主细胞自噬之间的关系目前尚未见报道。本项目拟在体外条件下，以绵羊肺炎支原体标准株Y98株分别感染鼠巨噬细胞系及鼠原代巨噬细胞，利用激光共聚焦扫描显微镜观察自噬体的形成、western blot检测自噬相关蛋白，探讨自噬在支原体感染过程中的形成机制；进一步检测巨噬细胞自噬对绵羊肺炎支原体的清除的影响；同时检测抗支原体感染免疫因子IFN-γ对巨噬细胞自噬的影响；并以支原体感染自噬抑制小鼠，检测体内条件下，自噬对该菌清除的影响。通过本项课题的开展，对自噬在绵羊肺炎支原体感染巨噬细胞中的作用及调控机制进行初步研究，并探讨体内条件下，自噬对支原体感染引发的免疫应答的影响。研究结果将有益于阐明绵羊肺炎支原体的致病机制及针对绵羊传染性胸膜肺炎的预防与治疗。

Contagious ovine pleuropneumoniae, caused by Mycoplasma ovipneumoniae, is the highly contagious disease. The study on the pathogenic mechanisms of M.ovipneumoniae is lagging behind, especially the relationship between M.ovipneumoniae with the host cell autophagy has not been reported.In the project, the murine macrophage cell line and primary mouse macrophages will be infected with M.ovipneumoniae Y98(the type strain)respectively in vitro.Then,using laser scanning confocal microscope to observe the formation of autophagysome, and western blot to detect autophagy-related proteins, we can know the formation mechanism and funtion of autophagy during M.ovipneumoniae infection;the influence of macrophage autophagy on killing mycoplasma ovipneumoniae and the effect of anti-mycoplasma infection immune factor IFN-γ on macrophage autophagy will be studied further;Using Y98 infecting autophage-inhibitted mice, we will study the impact of autophagy on immune response by M.ovipneumoniae in vivo.In the project, we will explore the role of autophagy in mycoplasma ovipneumoniae infection in macrophages and its regulation mechanism and in immune response elicited by M.ovipneumoniae infection preliminary in vivo. The results will be beneficial to elucidate the pathogenesis of M.ovipneumoniae and the prevention and treatment against contagious ovine pleuropneumoniae.