This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bain, C.
Right arrow Articles by Knutton, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bain, C.
Right arrow Articles by Knutton, S.

 Previous Article  |  Next Article 

Infect Immun, August 1998, p. 3900-3908, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Increased Levels of Intracellular Calcium Are Not Required for the Formation of Attaching and Effacing Lesions by Enteropathogenic and Enterohemorrhagic Escherichia coli

Christopher Bain,1 Rogeria Keller,2 Georgina K. Collington,1 Luiz R. Trabulsi,3 and Stuart Knutton1 *

Institute of Child Health, University of Birmingham, Birmingham B4 6NH, United Kingdom,1 and Departmento de Parasitologia, Instituto de Ciencias Biomedicas II, Universidade de Sao Paulo,2 and Laboratorio Especial de Microbiologia, Instituto Butantan,3 Sao Paulo, Brazil

Received 9 February 1998/Returned for modification 12 March 1998/Accepted 4 May 1998

Elevated concentrations of intracellular calcium ([Ca]i) have been implicated as an important signalling event during attaching and effacing (A/E) lesion formation by enteropathogenic Escherichia coli (EPEC). The highly localized nature of the cytoskeletal and cell surface alterations occurring during A/E lesion formation suggests that there should be equally localized EPEC-induced signalling events. To analyze further the calcium responses to infection of HEp-2 cells by EPEC, we employed calcium-imaging fluorescence microscopy, which allows both temporal and spatial measurements of [Ca]i in live cells. Using this imaging technique, not only were we unable to detect any significant elevation in [Ca]i at sites of A/E EPEC adhesion, but, with several different classical EPEC and enterohemorrhagic E. coli (EHEC) strains and three different infection procedures, each of which resulted in extensive A/E bacterial adhesion, we were unable to detect any significant alterations in [Ca]i in infected cells compared to uninfected cells. In addition, chelation of intracellular free calcium with bis-(aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA) did not, as previously reported, prevent A/E lesion formation. We conclude that increased [Ca]i are not required for A/E lesion formation by EPEC and EHEC.


* Corresponding author. Mailing address: Institute of Child Health, University of Birmingham, Clinical Research Block, Whittal St., Birmingham B4 6NH, United Kingdom. Phone: 44 121 333 8746. Fax: 44 121 333 8701. E-mail: S.KNUTTON{at}bham.ac.uk.


Infect Immun, August 1998, p. 3900-3908, Vol. 66, No. 8
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Brown, M. D., Bry, L., Li, Z., Sacks, D. B. (2008). Actin Pedestal Formation by Enteropathogenic Escherichia coli Is Regulated by IQGAP1, Calcium, and Calmodulin. J. Biol. Chem. 283: 35212-35222 [Abstract] [Full Text]  
  • Savkovic, S. D., Koutsouris, A., Hecht, G. (2003). PKC{zeta} participates in activation of inflammatory response induced by enteropathogenic E. coli. Am. J. Physiol. Cell Physiol. 285: C512-C521 [Abstract] [Full Text]  
  • Clarke, S. C., Haigh, R. D., Freestone, P. P. E., Williams, P. H. (2003). Virulence of Enteropathogenic Escherichia coli, a Global Pathogen. Clin. Microbiol. Rev. 16: 365-378 [Abstract] [Full Text]  
  • Ide, T., Michgehl, S., Knappstein, S., Heusipp, G., Schmidt, M. A. (2003). Differential Modulation by Ca2+ of Type III Secretion of Diffusely Adhering Enteropathogenic Escherichia coli. Infect. Immun. 71: 1725-1732 [Abstract] [Full Text]  
  • Lin, M., Zhu, M. X., Rikihisa, Y. (2002). Rapid Activation of Protein Tyrosine Kinase and Phospholipase C-{gamma}2 and Increase in Cytosolic Free Calcium Are Required by Ehrlichia chaffeensis for Internalization and Growth in THP-1 Cells. Infect. Immun. 70: 889-898 [Abstract] [Full Text]  
  • Savkovic, S. D., Ramaswamy, A., Koutsouris, A., Hecht, G. (2001). EPEC-activated ERK1/2 participate in inflammatory response but not tight junction barrier disruption. Am. J. Physiol. Gastrointest. Liver Physiol. 281: G890-G898 [Abstract] [Full Text]  
  • Jepson, M. A., Schlecht, H. B., Collares-Buzato, C. B. (2000). Localization of Dysfunctional Tight Junctions in Salmonella enterica Serovar Typhimurium-Infected Epithelial Layers. Infect. Immun. 68: 7202-7208 [Abstract] [Full Text]  
  • Phillips, A. D., Giròn, J., Hicks, S., Dougan, G., Frankel, G. (2000). Intimin from enteropathogenic Escherichia coli mediates remodelling of the eukaryotic cell surface. Microbiology 146: 1333-1344 [Abstract] [Full Text]