期刊文献+

VI型分泌系统2核心组分VgrG对禽致病性大肠杆菌致病性的影响 被引量:6

Effects of type VI secretion system 2 core component VgrG on the pathogenicity of avian Escherichia coli
原文传递
导出
摘要 【目的】构建禽致病性大肠杆菌(Avian pathogenic Escherichia coli,APEC)VI型分泌系统2(Type VI secretion system 2,T6SS2)结构基因vgrG缺失株,研究其对APEC生物学特性及致病性的影响。【方法】通过Red同源重组方法构建DE719菌株vgrG基因缺失株,并利用低拷贝质粒pSTV28构建互补株。比较分析野生株、缺失株与互补株的生长特性、运动性、生物被膜形成能力、黏附侵袭能力、动物致病力等差异。【结果】vgr G基因缺失不影响DE719的生长速度、运动能力及生物被膜形成能力。致病性试验表明缺失vgrG导致体内定殖能力及致病力显著下降,然而对DF-1细胞的黏附能力增强。【结论】T6SS2核心组分VgrG在APEC感染过程中发挥重要作用,为了解APEC的致病作用提供参考。 [Objective] To determine the role of type VI secretion system 2(T6SS2) core component VgrG in avian pathogenic Escherichia coli(APEC), we detected the biological characteristics and pathogenicity of APEC vgr G gene mutant strain. [Methods] We constructed the vgr G gene mutant strain and complementary strain of APEC DE719 by the Red recombination system and plasmid pSTV28. Then we analyzed the growth curve, motility, biofilm formation, adhesion and invasion capacity to DF-1 cells and virulence to duck of wild-type strain, mutant strain and complementary strain. [Results] The inactivation of vgr G gene did not affect the growth and motility, nor the biofilm formation of APEC. The vgr G gene mutant showed significantly decreased survival capacity and attenuated virulence in ducks. However, the adhesion capacity to DF-1 cells increased. [Conclusion] T6SS2 core component VgrG was involved in the process of APEC infection, which would help us to comprehensive understand the pathogenicity of APEC.
出处 《微生物学通报》 CAS CSCD 北大核心 2016年第9期2106-2113,共8页 Microbiology China
基金 国家自然科学基金项目(No.31572523 31370045) 公益性农业(科研)专项项目(No.201303044) 上海市科技兴农重点攻关项目(No.2015HNG1-9) 中央级科研院所基本科研业务费项目(No.2015JB08)~~
关键词 禽致病性大肠杆菌 vgrG基因 致病性 Avian pathogenic Escherichia coli vgrG gene Pathogenicity
  • 相关文献

参考文献21

  • 1Ron EZ. Host specificity of septicemic Escherichia coli: humanand avian pathogens[J]. Current Opinion in Microbiology, 2006,9(1):28-32.
  • 2Johnson JR, Russo TA. Extraintestinal pathogenic Escherichiacoli: “The other bad E. coir[i]. Journal of Laboratory andClinical Medicine, 2002,139(3): 155-162.
  • 3Schmidt H, Hensel M. Pathogenicity islands in bacterialpathogenesis[J]. Clinical Microbiology Reviews, 2004, 17(1):14-56.
  • 4Raj an I,Aravamuthan S, Maude SS. Identification ofcompositionally distinct regions in genomes using the centroidmethod[J]. Bioinformatics, 2007, 23(20): 2672-2677.
  • 5Cascales E. The type VI secretion tool kit[J]. EMBO Reports,2008,9(8): 735-741.
  • 6Filloux A, Hachani A, Bleves S. The bacterial type VI secretionmachine: yet another player for protein transport acrossmembranes[J]. Microbiology, 2008, 154(Pt 6): 1570-1583.
  • 7Shrivastava S, Mande SS. Identification and functionalcharacterization of gene components of Type VI Secretionsystem in bacterial genomes[J]. PLoS One, 2008, 3(8): e2955.
  • 8Dudley EG, Thomson NR, Parkhill J, et al. Proteomic andmicroarray characterization of the AggR regulon identifies apheU pathogenicity island in enteroaggregative Escherichiaco"[J]. Molecular Microbiology, 2006, 61(5): 1267-1282.
  • 9Pukatzki S, Ma AT, Revel AT, et al. Type VI secretion systemtranslocates a phage tail spike-like protein into target cellswhere it cross-links actin[J]. Proceedings of the NationalAcademy of Sciences of the United States of America, 2007,104(39): 15508*15513.
  • 10Zheng J, Leung KY. Dissection of a type VI secretion system inEdwardsiella tarda[J]. Molecular Microbiology, 2007, 66(5):1192-1206.

同被引文献33

引证文献6

二级引证文献14

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部