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Infection and Immunity, August 2009, p. 3234-3243, Vol. 77, No. 8
0019-9567/09/$08.00+0     doi:10.1128/IAI.00031-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Sab, a Novel Autotransporter of Locus of Enterocyte Effacement-Negative Shiga-Toxigenic Escherichia coli O113:H21, Contributes to Adherence and Biofilm Formation{triangledown}

Sylvia Herold, James C. Paton, and Adrienne W. Paton*

Research Centre for Infectious Diseases, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia

Received 8 January 2009/ Returned for modification 20 February 2009/ Accepted 21 May 2009

Shiga-toxigenic Escherichia coli (STEC) strains cause serious gastrointestinal disease, which can lead to potentially life-threatening systemic complications such as hemolytic-uremic syndrome. Although the production of Shiga toxin has been considered to be the main virulence trait of STEC for many years, the capacity to colonize the host intestinal epithelium is a crucial step in pathogenesis. In this study, we have characterized a novel megaplasmid-encoded outer membrane protein in locus of enterocyte effacement (LEE)-negative O113:H21 STEC strain 98NK2, termed Sab (for STEC autotransporter [AT] contributing to biofilm formation). The 4,296-bp sab gene encodes a 1,431-amino-acid protein with the features of members of the AT protein family. When expressed in E. coli JM109, Sab contributed to the diffuse adherence to human epithelial (HEp-2) cells and promoted biofilm formation on polystyrene surfaces. A 98NK2 sab deletion mutant was also defective in biofilm formation relative to its otherwise isogenic wild-type parent, and this was complemented by transformation with a sab-carrying plasmid. Interestingly, an unrelated O113:H21 STEC isolate that had a naturally occurring deletion in sab was similarly defective in biofilm formation. PCR analysis indicated that sab is present in LEE-negative STEC strains belonging to serotypes/groups O113:H21, O23, and O82:H8. These findings raise the possibility that Sab may contribute to colonization in a subset of LEE-negative STEC strains.

* Corresponding author. Mailing address: School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia. Phone: 61-8-83037552. Fax: 61-8-83033262. E-mail: adrienne.paton{at}adelaide.edu.au

{triangledown} Published ahead of print on 1 June 2009.

Editor: B. A. McCormick

Infection and Immunity, August 2009, p. 3234-3243, Vol. 77, No. 8
0019-9567/09/$08.00+0     doi:10.1128/IAI.00031-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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