Previous Article | Next Article ![]()
Infect. Immun., Mar 1996, 966-973, Vol 64, No. 3
I Rosenshine, S Ruschkowski and BB Finlay
Enteropathogenic Escherichia coli (EPEC) induces tyrosine phosphorylation
of a 90-kDa protein (Hp90) in infected epithelial cells. This in turn
facilitates intimate binding of EPEC via the outer membrane protein
intimin, effacement of host cell microvilli, cytoskeletal rearrangement,
and bacterial uptake. This phenotype has been commonly referred to as
attaching/effacing (A/E). The ability of EPEC to induce A/E lesions was
dependent on bacterial growth phase and temperature.
Early-logarithmic-phase EPEC grown at 37 degrees C elicits strong A/E
activity within minutes after infection of HeLa epithelial cells. EPEC de
novo protein syntheses during the first minutes of interaction with the
host cell was required to elicit A/E lesions. However, once formed,
bacterial viability was not needed to maintain A/E lesions. The type of
growth media and partial O2 pressure level do not seem to affect the
ability of EPEC to cause A/E lesions. These results indicates that the A/E
activity of EPEC is tightly regulated by environmental and host factors.
Copyright © 1996, American Society for Microbiology
Expression of attaching/effacing activity by enteropathogenic Escherichia coli depends on growth phase, temperature, and protein synthesis upon contact with epithelial cells
Department of Biotechnology and Molecular Genetics, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|