Shahzad W, Ajuwape Adebowale Titilayo Phillip, Rosenbusch Ricardo Francisco
Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, VMRI-5, 1802 University Boulevard, Ames, IA 50011, USA.
Vet Immunol Immunopathol. 2010 Jul;136(1-2):116-21. doi: 10.1016/j.vetimm.2010.02.001. Epub 2010 Feb 10.
Mycoplasma ovipneumoniae is associated with chronic non-progressive pneumonia of sheep and goats. As with many other mycoplasmas involved in animal diseases, protective immune responses have not been achieved with vaccines, even though antibody responses can be obtained. This study focuses on characterizing the interaction of M. ovipneumoniae with ovine PBMC using carboxy-fluorescein-succinimidyl-ester (CFSE) loading and flow cytometry to measure lymphoid cell division. M. ovipneumoniae induced a strong in vitro polyclonal suppression of CD4(+), CD8(+), and B blood lymphocyte subsets. The suppressive activity could be destroyed by heating to 60 degrees C, and partially impaired by formalin and binary ethyleneimine treatment that abolished its viability. The activity resided on the surface-exposed membrane protein fraction of the mycoplasma, since mild trypsin treatment not affecting viability was shown to reduce suppressive activity. Trypsin-treated mycoplasma regained suppressive activity once the mycoplasma was allowed to re-synthesize its surface proteins. Implications for the design of vaccines against M. ovipneumoniae are discussed.
绵羊肺炎支原体与绵羊和山羊的慢性非进行性肺炎有关。与许多其他引起动物疾病的支原体一样，尽管可以获得抗体反应，但疫苗尚未实现保护性免疫反应。本研究的重点是使用羧基荧光素琥珀酰亚胺酯（CFSE）加载和流式细胞术来测量淋巴细胞分裂，以表征绵羊肺炎支原体与绵羊外周血单核细胞（PBMC）的相互作用。绵羊肺炎支原体在体外对CD4(+)、CD8(+)和B血液淋巴细胞亚群诱导了强烈的多克隆抑制。加热至60摄氏度可破坏抑制活性，福尔马林和二乙烯亚胺处理可部分损害其活性，这两种处理均消除了其活力。该活性存在于支原体表面暴露的膜蛋白部分，因为已证明不影响活力的温和胰蛋白酶处理会降低抑制活性。一旦支原体被允许重新合成其表面蛋白，经胰蛋白酶处理的支原体就会恢复抑制活性。文中讨论了针对绵羊肺炎支原体疫苗设计的意义。
