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RfaH 增强了禽致病性大肠杆菌 O2 血清型 E058 菌株引起禽大肠杆菌病的能力。

RfaH promotes the ability of the avian pathogenic Escherichia coli O2 strain E058 to cause avian colibacillosis.

机构信息

Animal Infectious Disease Laboratory, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, People's Republic of China.

出版信息

J Bacteriol. 2013 Jun;195(11):2474-80. doi: 10.1128/JB.02074-12. Epub 2013 Mar 15.

Abstract

Avian pathogenic Escherichia coli (APEC) infection causes avian colibacillosis, which refers to any localized or systemic infection, such as acute fatal septicemia or subacute pericarditis and airsacculitis. The RfaH transcriptional regulator in E. coli is known to regulate a number of phenotypic traits. The direct effect of RfaH on the virulence of APEC has not been investigated yet. Our results showed that the inactivation of rfaH significantly decreased the virulence of APEC E058. The attenuation was assessed by in vivo and in vitro assays, including chicken infection assays, an ingestion and intracellular survival assay, and a bactericidal assay with serum complement. The virulence phenotype was restored to resemble that of the wild type by complementation of the rfaH gene in trans. The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) analysis and animal system infection experiments indicated that the deletion of rfaH correlated with decreased virulence of the APEC E058 strain.

摘要

禽致病性大肠杆菌(APEC)感染引起禽大肠杆菌病,是指任何局部或全身感染,如急性致命败血病或亚急性心包炎和气囊炎。大肠杆菌中的 RfaH 转录调节因子已知调节许多表型特征。然而,RfaH 对 APEC 毒力的直接影响尚未得到研究。我们的结果表明,rfaH 的失活显著降低了 APEC E058 的毒力。通过体内和体外试验评估衰减,包括鸡感染试验、摄取和细胞内存活试验以及血清补体杀菌试验。rfaH 基因的互补在转位上恢复了类似于野生型的毒力表型。定量实时逆转录-PCR(qRT-PCR)分析和动物系统感染实验的结果表明,rfaH 的缺失与 APEC E058 菌株毒力的降低相关。

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