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Sab, a Novel Autotransporter of Locus of Enterocyte Effacement-Negative Shiga-Toxigenic Escherichia coli O113:H21, Contributes to Adherence and Biofilm Formation

机译:Sab,一种新型的肠细胞表面阴性志贺毒素大肠埃希菌O113:H21的基因座自转运蛋白,有助于粘附和生物膜形成。

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Shiga-toxigenic Escherichia coli (STEC) strains cause serious gastrointestinal disease, which can lead to potentially life-threatening systemic complications such as hemolytic-uremic syndrome. Although the production of Shiga toxin has been considered to be the main virulence trait of STEC for many years, the capacity to colonize the host intestinal epithelium is a crucial step in pathogenesis. In this study, we have characterized a novel megaplasmid-encoded outer membrane protein in locus of enterocyte effacement (LEE)-negative O113:H21 STEC strain 98NK2, termed Sab (for STEC autotransporter [AT] contributing to biofilm formation). The 4,296-bp sab gene encodes a 1,431-amino-acid protein with the features of members of the AT protein family. When expressed in E. coli JM109, Sab contributed to the diffuse adherence to human epithelial (HEp-2) cells and promoted biofilm formation on polystyrene surfaces. A 98NK2 sab deletion mutant was also defective in biofilm formation relative to its otherwise isogenic wild-type parent, and this was complemented by transformation with a sab-carrying plasmid. Interestingly, an unrelated O113:H21 STEC isolate that had a naturally occurring deletion in sab was similarly defective in biofilm formation. PCR analysis indicated that sab is present in LEE-negative STEC strains belonging to serotypes/groups O113:H21, O23, and O82:H8. These findings raise the possibility that Sab may contribute to colonization in a subset of LEE-negative STEC strains.
机译:志贺毒素大肠杆菌(STEC)菌株引起严重的胃肠道疾病,可导致潜在的危及生命的全身性并发症,例如溶血性尿毒症综合征。尽管多年来一直认为志贺毒素的产生是STEC的主要毒力特征,但定殖宿主肠道上皮的能力是发病机理中的关键步骤。在这项研究中,我们已经表征了一种新的大质粒编码的外膜蛋白,位于肠上皮细胞侵染(LEE)阴性的O113:H21 STEC菌株98NK2的基因座中,称为Sab(对于STEC自转运蛋白[AT]有助于生物膜形成)。 4296 bp的 sab 基因编码一个具有AT蛋白质家族成员特征的1,431个氨基酸的蛋白质。用 E表示。大肠杆菌JM109,Sab促进了对人类上皮(HEp-2)细胞的弥散粘附,并促进了聚苯乙烯表面上生物膜的形成。相对于其同基因的野生型亲本,一个98NK2 sab 缺失突变体在生物膜形成方面也有缺陷,并且可以通过携带 sab 的质粒转化来补充。有趣的是,在 sab 中具有天然缺失的不相关的O113:H21 STEC分离物在生物膜形成中同样具有缺陷。 PCR分析表明, sab 存在于血清型/组O113:H21,O23和O82:H8的LEE阴性STEC菌株中。这些发现增加了Sab可能在LEE阴性STEC菌株亚群中定植的可能性。

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