Donnenberg M S, Calderwood S B, Donohue-Rolfe A, Keusch G T, Kaper J B
Department of Medicine, University of Maryland School of Medicine, Baltimore 21201.
Infect Immun. 1990 Jun;58(6):1565-71. doi: 10.1128/iai.58.6.1565-1571.1990.
Enteropathogenic Escherichia coli (EPEC) strains have recently been shown to invade tissue culture cells. We describe a set of 22 Tn5 IS50L::phoA (TnphoA) insertion mutants of EPEC strain E2348-69 that are unable to invade HEp-2 cells. Each mutant was tested for the ability to adhere to and to induce the polymerization of actin in HEp-2 cells. Southern hybridization of plasmid and total DNA of each strain was performed to determine the location of each TnphoA insert, and each TnphoA insert along with flanking EPEC sequences was cloned. These studies resulted in the grouping of the mutants into five main categories. These include strains with plasmid and chromosomal insertions that alter adherence, chromosomal insertions that alter the ability to induce actin polymerization, and chromosomal insertions that do not affect adherence or actin polymerization. These studies indicate that genes affecting EPEC adherence may be located on both the plasmid and chromosome, that several genes are involved in the induction of actin polymerization in epithelial cells, and that EPEC invasion is a complex process involving multiple genetic loci.
肠道致病性大肠杆菌（EPEC）菌株最近已被证明能够侵入组织培养细胞。我们描述了一组22个EPEC菌株E2348 - 69的Tn5 IS50L::phoA（TnphoA）插入突变体，它们无法侵入HEp - 2细胞。对每个突变体进行了在HEp - 2细胞中黏附及诱导肌动蛋白聚合的能力测试。对每个菌株的质粒和总DNA进行了Southern杂交，以确定每个TnphoA插入的位置，并克隆了每个TnphoA插入片段及其侧翼的EPEC序列。这些研究导致突变体被分为五大类。其中包括质粒和染色体插入导致黏附改变的菌株、染色体插入导致诱导肌动蛋白聚合能力改变的菌株，以及染色体插入不影响黏附或肌动蛋白聚合的菌株。这些研究表明，影响EPEC黏附的基因可能位于质粒和染色体上，多个基因参与上皮细胞中肌动蛋白聚合的诱导，并且EPEC的侵入是一个涉及多个基因位点的复杂过程。
