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 Luck, S. N.
Right arrow Articles by Hartland, E. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Luck, S. N.
Right arrow Articles by Hartland, E. L.

 Previous Article  |  Next Article 

Infection and Immunity, December 2006, p. 6999-7004, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.00435-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21{triangledown}

Shelley N. Luck,1 Luminita Badea,1 Vicki Bennett-Wood,2 Roy Robins-Browne,2 and Elizabeth L. Hartland1*

Australian Bacterial Pathogenesis Program, Department of Microbiology, Monash University, Melbourne, Victoria 3800,1 Australian Bacterial Pathogenesis Program, Department of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria 3010, Australia2

Received 17 March 2006/ Returned for modification 26 April 2006/ Accepted 24 August 2006

Enterohemorrhagic Escherichia coli (EHEC) O113:H21 can invade epithelial cells. In this study, we found that invasion but not adherence was inhibited by anti-FliCH21 specific antibodies. In addition, deletion of fliCH21 from EHEC O113:H21 resulted in an eightfold decrease in invasion that was restored upon transcomplementation with fliCH21 but not with fliCH6. These results suggested that FliC plays an important role in the pathogenesis of infections caused by EHEC O113:H21 by allowing bacteria to penetrate the intestinal epithelium.


* Corresponding author. Mailing address: Department of Microbiology, Monash University, Clayton 3800, Victoria, Australia. Phone: (61) 3 9905 4323. Fax: (61) 3 9905 4811. E-mail: Liz.Hartland{at}med.monash.edu.au.

{triangledown} Published ahead of print on 18 September 2006.

Editor: J. B. Bliska


Infection and Immunity, December 2006, p. 6999-7004, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.00435-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Sampaio, S. C. F., Gomes, T. A. T., Pichon, C., du Merle, L., Guadagnini, S., Abe, C. M., Sampaio, J. L. M., Le Bouguenec, C. (2009). The Flagella of an Atypical Enteropathogenic Escherichia coli Strain Are Required for Efficient Interaction with and Stimulation of Interleukin-8 Production by Enterocytes In Vitro. Infect. Immun. 77: 4406-4413 [Abstract] [Full Text]  
  • Xicohtencatl-Cortes, J., Monteiro-Neto, V., Saldana, Z., Ledesma, M. A., Puente, J. L., Giron, J. A. (2009). The Type 4 Pili of Enterohemorrhagic Escherichia coli O157:H7 Are Multipurpose Structures with Pathogenic Attributes. J. Bacteriol. 191: 411-421 [Abstract] [Full Text]