New Role for the ibeA Gene in H2O2 Stress Resistance of Escherichia coli
New Role for the ibeA Gene in H2O2 Stress Resistance of Escherichia coli
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DOI：
10.1128/jb.00089-12
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发表时间：
2012-09-01
影响因子：
3.2
通讯作者：
Germon, Pierre
中科院分区：
文献类型：
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作者：
Flechard, Maud;Cortes, Melanie A. M.;Germon, Pierre
ibeA是在来自B2系统发育群的一些肠外致病性大肠杆菌（ExPEC）菌株中发现的毒力因子，特别是在新生脑膜炎和禽类致病性菌株中。它被证明参与新生脑膜炎菌株RS 218的侵袭过程。在以前的工作中，我们表明，在禽致病性E。大肠杆菌（APEC）菌株BEN 2908中，ibeA通过调节1型菌毛的合成而参与粘附真核细胞（M. A.科尔特斯等人，Infect. Immun. 76：4129-4136，2008）。在这项研究中，我们证明了ibeA在抗氧化应激中的新作用。结果表明，E. coli BEN 2908对H2 O2的杀伤作用比野生型更敏感。在携带ibeA的整个GimA基因组区域缺失的突变体中也观察到这种表型，并且可能与参与氧化应激反应的基因子集的表达改变有关。我们还表明，RpoS表达没有改变ibeA缺失。此外，将ibeA表达质粒转入E.表达或不表达1型菌毛的大肠杆菌K-12菌株对H_2O_2攻击具有更强的抗性。总之，这些结果表明ibeA本身能够赋予E.杆菌这一特征可以部分解释ibeA在致病菌株毒力中所起的作用。
ibeA is a virulence factor found in some extraintestinal pathogenic Escherichia coli (ExPEC) strains from the B2 phylogenetic group and particularly in newborn meningitic and avian pathogenic strains. It was shown to be involved in the invasion process of the newborn meningitic strain RS218. In a previous work, we showed that in the avian pathogenic E. coli (APEC) strain BEN2908, isolated from a colibacillosis case, ibeA was rather involved in adhesion to eukaryotic cells by modulating type 1 fimbria synthesis (M. A. Cortes et al., Infect. Immun. 76:4129-4136, 2008). In this study, we demonstrate a new role for ibeA in oxidative stress resistance. We showed that an ibeA mutant of E. coli BEN2908 was more sensitive than its wild-type counterpart to H2O2 killing. This phenotype was also observed in a mutant deleted for the whole GimA genomic region carrying ibeA and might be linked to alterations in the expression of a subset of genes involved in the oxidative stress response. We also showed that RpoS expression was not altered by the ibeA deletion. Moreover, the transfer of an ibeA-expressing plasmid into an E. coli K-12 strain, expressing or not expressing type 1 fimbriae, rendered it more resistant to an H2O2 challenge. Altogether, these results show that ibeA by itself is able to confer increased H2O2 resistance to E. coli. This feature could partly explain the role played by ibeA in the virulence of pathogenic strains.