滑液支原体（MS）为OIE须通报禽病病原，可导致传染性滑膜炎、生长迟缓等，严重危害我国家禽养殖业。前期研究发现MS诱发鸡滑膜炎时在病变滑膜处的菌体载量显著高于其他部位；MS粘附腱鞘滑膜细胞（TSSC）显著增强该细胞的炎症反应；MS的EF-G可在外膜锚定，并显著促进MS粘附TSSC。目前MS粘附TSSC的分子机制不明确。在已有工作基础上，申请者拟通过Pull-Down、高通量质谱等方法筛选和鉴定EF-G在TSSC的表面受体；结合二甲基修饰、质谱技术等研究EF-G在MS的膜锚定分段形式，揭示外膜锚定EF-G发挥粘附作用、与受体结合的关键区段/位点；利用受体抗体封闭、siRNA干扰等手段揭示EF-G与受体的结合在EF-G促进MS粘附TSSC及在粘附所致炎症反应中的作用。研究结果将解析外膜锚定EF-G促进MS粘附TSSC的分子机制，以利于进一步研究MS定植腱鞘滑膜并导致滑膜炎的机制。

Mycoplasma synoviae (MS) is an avian pathogen of the OIE statutory list of notifiable diseases. MS can cause synovitis, growth retardation, etc., which seriously endangers the poultry farming in China. Previous studies showed that the MS loads from the diseased synovial tissues were significantly higher than other organs when the chicken suffered from synovitis caused by the MS. The adhesion of MS to tendon sheath synovial cells (TSSC) significantly stimulated TSSC to produce an inflammatory response. MS EF-G anchored on the outer membrane of MS, which significantly promoted MS adhesion to TSSC. At present, the molecular mechanism of MS adhesion to TSSC is not clear. Based on the existing work, the applicant intends to focus on the screening and identification of the surface receptors of EF-G in TSSC by Pull-Down, high-throughput mass spectrometry, and other methods. Study the specific segmentation of EF-G's membrane anchoring in MS using dimethyl modification, mass spectrometry, and other techniques, in order to reveal the key segments/sites of outer membrane-anchored EF-G with adhesion and receptor binding capacity. Besides, receptor antibody blocking, siRNA interference, and other means are used to reveal the role of EF-G binding to the receptor in EF-G promoting MS adhesion to TSSC and adhesion-induced inflammation. The results of the study will analyze the molecular mechanism of surface-anchored EF-G to promote MS adhesion to TSSC, so as to further study the mechanism of MS colonization of tendon sheath synovium and lead to synovitis.