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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Invasiveness as a putative additional virulence mechanism of some atypical Enteropathogenic Escherichia coli strains with different uncommon intimin types

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Author(s):
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Yamamoto, Denise [1, 2] ; Hernandes, Rodrigo T. [1, 2] ; Blanco, Miguel [3] ; Greune, Lilo [2] ; Schmidt, M. Alexander [2] ; Carneiro, Sylvia M. [4] ; Dahbi, Ghizlane [3] ; Blanco, Jesus E. [3] ; Mora, Azucena [3] ; Blanco, Jorge [3] ; Gomes, Tania A. T. [1]
Total Authors: 11
Affiliation:
[1] Univ Fed Sao Paulo, BR-04023062 Sao Paulo - Brazil
[2] Univ Munster, Inst Infektiol, Zentrum Mol Biol Entzundung, Munster - Germany
[3] Univ Santiago de Compostela, Fac Vet, Dept Microbiol & Parasitol, E Coli Reference Lab LREC, Lugo - Spain
[4] Inst Butantan, Lab Biol Celular, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: BMC Microbiology; v. 9, JUL 21 2009.
Web of Science Citations: 24
Abstract

Background: Enteropathogenic Escherichia coli (EPEC) produce attaching/effacing (A/E) lesions on eukaryotic cells mediated by the outer membrane adhesin intimin. EPEC are sub-grouped into typical (tEPEC) and atypical (aEPEC). We have recently demonstrated that aEPEC strain 1551-2 (serotype O non-typable, non-motile) invades HeLa cells by a process dependent on the expression of intimin sub-type omicron. In this study, we evaluated whether aEPEC strains expressing other intimin sub-types are also invasive using the quantitative gentamicin protection assay. We also evaluated whether aEPEC invade differentiated intestinal T84 cells. Results: Five of six strains invaded HeLa and T84 cells in a range of 13.3%-20.9% and 5.8%-17.8%, respectively, of the total cell-associated bacteria. The strains studied were significantly more invasive than prototype tEPEC strain E2348/69 (1.4% and 0.5% in HeLa and T84 cells, respectively). Invasiveness was confirmed by transmission electron microscopy. We also showed that invasion of HeLa cells by aEPEC 1551-2 depended on actin filaments, but not on microtubules. In addition, disruption of tight junctions enhanced its invasion efficiency in T84 cells, suggesting preferential invasion via a non-differentiated surface. Conclusion: Some aEPEC strains may invade intestinal cells in vitro with varying efficiencies and independently of the intimin sub-type. (AU)