The Shmunis School of Biomedicine and Cancer Research, Faculty of Life Sciences, Tel Aviv Universitygrid.12136.37, Tel Aviv, Israel.
Institute for Microbiology, University of Greifswald, Greifswald, Germany.
Infect Immun. 2021 Sep 16;89(10):e0031621. doi: 10.1128/IAI.00316-21. Epub 2021 Jun 28.
Extraintestinal pathogenic Escherichia coli (ExPEC) strains constitute a serious and emerging clinical problem, as they cause a variety of infections and are usually highly antibiotic resistant. Many ExPEC strains are capable of evading the bactericidal effects of serum and causing sepsis. One critical factor for the development of septicemia is the increased serum survival () gene, which is highly correlated with complement resistance and lethality. Although it is very important, the function of the gene has not been elucidated so far. We have been studying the serum survival of a septicemic strain of E. coli serotype O78, which has a group 4 capsule. Here, we show that the gene is required for the synthesis of capsules, which protect the bacteria from the bactericidal effect of complement. Moreover, we show that the deletion of the gene results in significantly increased binding of the complement proteins that constitute the membrane attack complex to the bacterial surface.
肠外致病性大肠杆菌(ExPEC)菌株构成了一个严重且不断出现的临床问题,因为它们会引起多种感染,并且通常具有高度的抗生素耐药性。许多 ExPEC 菌株能够逃避血清的杀菌作用并导致败血症。引发败血症的一个关键因素是血清存活()基因的增加,该基因与补体抗性和致死性高度相关。尽管这一点非常重要,但迄今为止,基因的功能尚未阐明。我们一直在研究大肠杆菌 O78 血清型的败血症菌株的血清存活能力,该菌株具有 4 组荚膜。在这里,我们表明基因对于荚膜的合成是必需的,荚膜可以保护细菌免受补体的杀菌作用。此外,我们还表明,基因缺失会导致构成膜攻击复合物的补体蛋白与细菌表面的结合显著增加。