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 Ludwig, A.
Right arrow Articles by Goebel, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ludwig, A.
Right arrow Articles by Goebel, W.

 Previous Article  |  Next Article 

Journal of Bacteriology, August 2004, p. 5311-5320, Vol. 186, No. 16
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.16.5311-5320.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Molecular Analysis of Cytolysin A (ClyA) in Pathogenic Escherichia coli Strains

Albrecht Ludwig,1* Christine von Rhein,1 Susanne Bauer,2 Christian Hüttinger,1,2,{dagger} and Werner Goebel2

Institut für Medizinische Mikrobiologie, Klinikum der Johann Wolfgang Goethe-Universität, 60596 Frankfurt am Main,1 Lehrstuhl für Mikrobiologie, Theodor-Boveri-Institut für Biowissenschaften (Biozentrum), Universität Würzburg, Am Hubland, 97074 Würzburg, Germany2

Received 5 December 2003/ Accepted 12 May 2004

Cytolysin A (ClyA) of Escherichia coli is a pore-forming hemolytic protein encoded by the clyA (hlyE, sheA) gene that was first identified in E. coli K-12. In this study we examined various clinical E. coli isolates with regard to the presence and integrity of clyA. PCR and DNA sequence analyses demonstrated that 19 of 23 tested Shiga toxin-producing E. coli (STEC) strains, all 7 tested enteroinvasive E. coli (EIEC) strains, 6 of 8 enteroaggregative E. coli (EAEC) strains, and 4 of 7 tested enterotoxigenic E. coli (ETEC) strains possess a complete clyA gene. The remaining STEC, EAEC, and ETEC strains and 9 of the 17 tested enteropathogenic E. coli (EPEC) strains were shown to harbor mutant clyA derivatives containing 1-bp frameshift mutations that cause premature termination of the coding sequence. The other eight EPEC strains and all tested uropathogenic and new-born meningitis-associated E. coli strains (n = 14 and 3, respectively) carried only nonfunctional clyA fragments due to the deletion of two sequences of 493 bp and 204 or 217 bp at the clyA locus. Expression of clyA from clinical E. coli isolates proved to be positively controlled by the transcriptional regulator SlyA. Several tested E. coli strains harboring a functional clyA gene produced basal amounts of ClyA when grown under standard laboratory conditions, but most of them showed a clyA-dependent hemolytic phenotype only when SlyA was overexpressed. The presented data indicate that cytolysin A can play a role only for some of the pathogenic E. coli strains.

* Corresponding author. Mailing address: Institut für Medizinische Mikrobiologie, Klinikum der Johann Wolfgang Goethe-Universität, Paul-Ehrlich-Straße 40, 60596 Frankfurt am Main, Germany. Phone: (49) 69 6301 7165. Fax: (49) 69 6301 5767. E-mail: albrecht.ludwig{at}em.uni-frankfurt.de.

{dagger} Present address: Institut für Molekulare Infektionsbiologie, Universität Würzburg, 97070 Würzburg, Germany.

Journal of Bacteriology, August 2004, p. 5311-5320, Vol. 186, No. 16
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.16.5311-5320.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Highet, A. R., Berry, A. M., Bettelheim, K. A., Goldwater, P. N. (2009). The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants. J Med Microbiol 58: 285-289 [Abstract] [Full Text]  
  • Faucher, S. P., Forest, C., Beland, M., Daigle, F. (2009). A novel PhoP-regulated locus encoding the cytolysin ClyA and the secreted invasin TaiA of Salmonella enterica serovar Typhi is involved in virulence. Microbiology 155: 477-488 [Abstract] [Full Text]  
  • Fagerlund, A., Lindback, T., Storset, A. K., Granum, P. E., Hardy, S. P. (2008). Bacillus cereus Nhe is a pore-forming toxin with structural and functional properties similar to the ClyA (HlyE, SheA) family of haemolysins, able to induce osmotic lysis in epithelia. Microbiology 154: 693-704 [Abstract] [Full Text]  
  • Hunt, S., Moir, A. J. G., Tzokov, S., Bullough, P. A., Artymiuk, P. J., Green, J. (2008). The formation and structure of Escherichia coli K-12 haemolysin E pores. Microbiology 154: 633-642 [Abstract] [Full Text]  
  • Turner, S. M., Chaudhuri, R. R., Jiang, Z.-D., DuPont, H., Gyles, C., Penn, C. W., Pallen, M. J., Henderson, I. R. (2006). Phylogenetic Comparisons Reveal Multiple Acquisitions of the Toxin Genes by Enterotoxigenic Escherichia coli Strains of Different Evolutionary Lineages. J. Clin. Microbiol. 44: 4528-4536 [Abstract] [Full Text]  
  • von Rhein, C., Hunfeld, K.-P., Ludwig, A. (2006). Serologic Evidence for Effective Production of Cytolysin A in Salmonella enterica Serovars Typhi and Paratyphi A during Human Infection. Infect. Immun. 74: 6505-6508 [Abstract] [Full Text]  
  • Muller, C. M., Dobrindt, U., Nagy, G., Emody, L., Uhlin, B. E., Hacker, J. (2006). Role of Histone-Like Proteins H-NS and StpA in Expression of Virulence Determinants of Uropathogenic Escherichia coli.. J. Bacteriol. 188: 5428-5438 [Abstract] [Full Text]  
  • Kerenyi, M., Allison, H. E., Batai, I., Sonnevend, A., Emody, L., Plaveczky, N., Pal, T. (2005). Occurrence of hlyA and sheA Genes in Extraintestinal Escherichia coli Strains. J. Clin. Microbiol. 43: 2965-2968 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»