摘要
构建禽致病性大肠杆菌(APEC)Ⅵ型分泌系统2(T6SS2)clpB基因缺失株、互补株,研究clpB基因对APEC生物学特性及致病性的影响。采用Red同源重组系统构建APEC clpB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曲线、运动性、生物被膜形成能力、黏附侵袭能力、胞内存活能力、动物致病力等生物学特性的差异。结果显示,clpB基因缺失不影响APEC的生长速度和黏附侵袭能力。然而,缺失ClpB导致APEC运动能力降低、生物被膜形成能力升高、HD-11胞内存活能力降低、体内存活能力及致病力降低。本研究分析了T6SS2核心组分Clp B的作用,为阐述APEC T6SS2致病作用提供了参考。
To determine the roles of type Visecretion system 2（T6SS2）core component clpBin avian pathogenic Escherichia coli（APEC）,we detected the biological characteristics and pathogenicity of APEC clpBgene mutant and complementary strains. We constructed the clpBgene mutant strain and complementary strain of APEC DE719 by Red recombination system and low-copy plasmid pSTV28. Then we compared and analyzed the growth curve,motility,biofilm formation,adhesion and invasion capacity,intracellular survival capacity and virulence to duck of wild-type strain,mutant strain and complementary strain. The results showed that inactivation of clpB gene did not affect the growth,nor the adhesion and invasion capacities of APEC. The biofilm formation of clpB mutant strain was increased. However,the clpBgene mutant showed significantly decreased motility,survival capacity and attenuated virulence in ducks. This study showed the roles of T6SS2 core component ClpB,which would help us to comprehensively understand the pathogenicity of T6SS2 in APEC.
出处
《中国兽医科学》
CAS
CSCD
北大核心
2016年第7期834-840,共7页
Chinese Veterinary Science
基金
国家自然科学基金项目(31572523
31370045)
公益性农业(科研)专项项目(201303044)
上海市科技兴农重点攻关项目(沪农科攻字2015第1-9号)
