作 者: ; ; ; ; ; ; ; ; ; (吴小卡); (胡剑刚);
机构地区: 中国农业科学院上海兽医研究所
出 处: 《中国兽医科学》 2016年第11期1432-1437,共6页
摘 要: 为研究sfs A基因对禽致病性大肠杆菌(APEC)生物学特性的影响,利用Red重组方法构建禽致病性大肠杆菌APEC94株的sfs A基因缺失株,分析野生株与缺失株在生长特性、黏附和入侵D F-1细胞及生物被膜形成等生物学特性上的差异。通过动物试验,评价sfs A在APEC感染樱桃谷鸭过程中的作用。结果表明,sfs A缺失不影响APEC94菌株的生长特性和黏附、入侵DF-1细胞能力,但缺失株的生物被膜形成能力明显下降(P<0.000 1)。动物试验结果表明,与野生株相比,sfs A缺失株在樱桃谷鸭肝中的细菌载量显著降低(P<0.05),而在肾、脾和血液中无显著下降(P>0.05)。结果显示,sfs A基因的缺失显著降低禽致病性大肠杆菌的生物被膜形成能力及其在肝中的细菌载量,推测sfs A基因可能参与APEC对宿主的致病性。 To study the role of sfsA gene in avian pathogenic Escherichia coli(APEC),the sfsA mutant strain was constructed by homologous recombination assay. The growth characteristics,ability of adhe sion and invasion to DF-1 cells,formation of biofilm,median lethal dose(LD50) and the bacterial loads in vivo were analyzed between the sfsA mutant strain and the wild strain. There was no significant differ- ence in growth curve,and the ability of adhesion and invasion to DF-I cells between the wide strain and the mutant strain. However,the ability of biofilm formation of the sfsA mutant strain decreased obvi- ously compared with the wild strain(P〈0. 05). Furthermore,in vivo studies showed that the bacterial loads of the sfsAmutant strain was significantly decreased in the liver(P〈0. 05),while the study re- sults showed no significantly difference in spleen,kidney and blood in infected ducks. The deletion ofsfsA could abate the biofilm formation ability,and decrease the bacterial loads in liver in duck,which showed that the sfsA gene play roles in pathogenicity of APEC.