Xie Fang, Li Gang, Zhang Wanjiang, Zhang Yanhe, Zhou Long, Liu Shuanghong, Liu Siguo, Wang Chunlai
State Key Laboratory of Veterinary Biotechnology, Division of Bacterial Diseases, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 15001, People's Republic of China.
State Key Laboratory of Veterinary Biotechnology, Division of Bacterial Diseases, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 15001, People's Republic of China.
Vet Microbiol. 2016 Feb 1;183:1-8. doi: 10.1016/j.vetmic.2015.11.021. Epub 2015 Nov 22.
The outer membrane proteins of Actinobacillus pleuropneumoniae are mediators of infection, acting as targets for the host's defense system. The outer membrane lipoprotein VacJ is involved in serum resistance and intercellular spreading in several pathogenic bacteria. To investigate the role of VacJ in the pathogenicity of Actinobacillus pleuropneumoniae, the vacJ gene-deletion mutant MD12 ΔvacJ was constructed. The increased susceptibility to KCl, SDS plus EDTA, and several antibiotics in the MD12ΔvacJ mutant suggested that the stability of the outer membrane was impaired as a result of the mutation in the vacJ gene. The increased NPN fluorescence and significant cellular morphological variation in the MD12ΔvacJ mutant further demonstrated the crucial role of the VacJ lipoprotein in maintaining the outer membrane integrity of A. pleuropneumoniae. In addition, the MD12ΔvacJ mutant exhibited decreased survival from the serum and complement killing compared to the wild-type strain. Interestingly, the MD12ΔvacJ mutant showed reduced biofilm formation compared to the wild-type strain. To our knowledge, this is the first description of the VacJ lipoprotein contributing to bacterial biofilm formation. The data presented in this study illustrate the important role of the VacJ lipoprotein in the maintenance of cellular integrity, serum resistance, and biofilm formation in A. pleuropneumoniae.
胸膜肺炎放线杆菌的外膜蛋白是感染的介质，可作为宿主防御系统的靶标。外膜脂蛋白VacJ在几种病原菌的血清抗性和细胞间传播中起作用。为了研究VacJ在胸膜肺炎放线杆菌致病性中的作用，构建了vacJ基因缺失突变体MD12ΔvacJ。MD12ΔvacJ突变体对氯化钾、十二烷基硫酸钠加乙二胺四乙酸以及几种抗生素的敏感性增加，这表明vacJ基因突变导致外膜稳定性受损。MD12ΔvacJ突变体中NPN荧光增加和明显的细胞形态变化进一步证明了VacJ脂蛋白在维持胸膜肺炎放线杆菌外膜完整性中的关键作用。此外，与野生型菌株相比，MD12ΔvacJ突变体在血清和补体杀伤中的存活率降低。有趣的是，与野生型菌株相比，MD12ΔvacJ突变体的生物膜形成减少。据我们所知，这是关于VacJ脂蛋白促进细菌生物膜形成的首次描述。本研究提供的数据说明了VacJ脂蛋白在维持胸膜肺炎放线杆菌细胞完整性、血清抗性和生物膜形成中的重要作用。
