A hybrid protein containing MSP1a repeats and Omp7, Omp8 and Omp9 epitopes protect immunized BALB/c mice against anaplasmosis

含有 MSP1a 重复序列和 Omp7、Omp8 和 Omp9 表位的混合蛋白可保护免疫的 BALB/c 小鼠免受无形体病的侵害

阅读:7
作者:Alex Sander R Cangussu, Luis André M Mariúba, Pritesh Lalwani, Keila Dayane E S Pereira, Spartaco Astolphi-Filho, Patricia P Orlandi, Sabrina Epiphanio, Kelvison F Viana, Mucio Flavio B Ribeiro, Hidelberto M Silva, Claudio R F Marinho, Paulo A Nogueira

Abstract

Anaplasma marginale (A. marginale) has a remarkable impact on livestock production, and an effective vaccine is not currently available due to the inexistence of a small animal model. Recently, BALB/c mice were successfully infected with A. marginale, resulting in an acute and persistent anaplasmosis infection. Here, we designed a hybrid protein containing repeats of polypeptide 1a from major surface protein-1 complex (MSP1a) repeats and common epitopes of outer membrane proteins (OMPs) OMP7, OMP8 and OMP9 expressed in Escherichia coli. Our proof-of-concept assessed vaccinal effectiveness against a challenge with live bacteria. The MSP1a/OMP7/8/9 immunized BALB/C mice exhibited a strong reduction in rickettsemia and had no signs of anaplasmosis or hepatic lesions. In contrast, the non-immunized mice exhibited signs of anaplasmosis and a body weight loss associated with increases in monocyte and neutrophil counts. Furthermore, the non-immunized mice displayed atrophies with chronic inflammatory infiltrates in the spleen and increased binucleation and hydropic degeneration in the hepatocytes. Our findings demonstrated that immunization with our hybrid protein induced a strong reduction in rickettsemia and conferred protection against anaplasmosis. Therefore, given the strong evidence of the protective effect against anaplasmosis, hybrid protein designs are potential candidates for the rational design of vaccinal subunits.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。