一些致病性大肠杆菌（EPEC）临床分离株中束状菌毛表达缺失是由于bfp操纵子中一个保守的大片段缺失。

Lack of expression of bundle-forming pili in some clinical isolates of enteropathogenic Escherichia coli (EPEC) is due to a conserved large deletion in the bfp operon.

作者信息

Bortolini M R, Trabulsi L R, Keller R, Frankel G, Sperandio V

机构信息

Instituto de Ciências Biomédicas, Departamento de Microbiologia, Universidade de São Paulo, Av. Prof Lineu Prestes, 1374 CEP:05389-970, São Paulo, Brazil.

出版信息

FEMS Microbiol Lett. 1999 Oct 1;179(1):169-74. doi: 10.1111/j.1574-6968.1999.tb08723.x.

DOI:10.1111/j.1574-6968.1999.tb08723.x

PMID:10481102

Abstract

Enteropathogenic Escherichia coli (EPEC) produces a plasmid-encoded type IV pilus, called the bundle-forming pilus (BFP), involved in the formation of the localized adhesion onto epithelial cells. In this study, we demonstrate that clinical isolates of serotypes O128ab:H2 and O119:H2 contain a ca. 13-kb deletion in the bfp operon, resulting in a lack of expression of these pili. An IS sequence with homology to the IS66 of Agrobacterium tumefaciens replaced the deleted bfp genes. These results suggest that the bfp operon was deleted through a transpositional event and that other adherence factors may mediate attachment of these bacteria to the host cells.

摘要

肠致病性大肠杆菌（EPEC）产生一种由质粒编码的IV型菌毛，称为束状菌毛（BFP），它参与在上皮细胞上形成局部黏附。在本研究中，我们证明血清型O128ab:H2和O119:H2的临床分离株在bfp操纵子中存在约13 kb的缺失，导致这些菌毛缺乏表达。一个与根癌农杆菌IS66具有同源性的IS序列取代了缺失的bfp基因。这些结果表明，bfp操纵子是通过转座事件缺失的，并且其他黏附因子可能介导这些细菌与宿主细胞的附着。