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Infection and Immunity, December 2008, p. 5598-5607, Vol. 76, No. 12
0019-9567/08/$08.00+0 doi:10.1128/IAI.01180-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

ZAP Lab, Division of Immunity and Infection, The Roslin Institute and R(D)SVS, Chancellor's Building, University of Edinburgh, Edinburgh EH16 4SB, United Kingdom,1 Scottish E. coli O157 Reference Laboratory, Department of Clinical Microbiology, Western General Hospital, Edinburgh EH4 2XU, United Kingdom,2 Animal Health Group, Research Division, SAC, Kings Buildings, Edinburgh EH9 3JG, United Kingdom,3 Department of Food and Environmental Safety, Veterinary Laboratories Agency, Weybridge, New Haw, Addlestone KT15 3NB, United Kingdom4
Received 23 September 2008/ Accepted 25 September 2008
Non-sorbitol-fermenting (NSF) Escherichia coli O157:H7 is the primary Shiga toxin-producing E. coli (STEC) serotype associated with human infection. Since 1988, sorbitol-fermenting (SF) STEC O157:NM strains have emerged and have been associated with a higher incidence of progression to hemolytic-uremic syndrome (HUS) than NSF STEC O157:H7. This study investigated bacterial factors that may account for the increased pathogenic potential of SF STEC O157:NM. While no evidence of toxin or toxin expression differences between the two O157 groups was found, the SF STEC O157:NM strains adhered at significantly higher levels to a human colonic cell line. Under the conditions tested, curli were shown to be the main factor responsible for the increased adherence to Caco-2 cells. Notably, 52 of 66 (79%) European SF STEC O157:NM strains tested bound Congo red at 37oC and this correlated with curli expression. In a subset of strains, curli expression was due to increased expression from the csgBAC promoter that was not always a consequence of increased csgD expression. The capacity of SF STEC O157:NM strains to express curli at 37oC may have relevance to the epidemiology of human infections as curliated strains could promote higher levels of colonization and inflammation in the human intestine. In turn, this could lead to increased toxin exposure and an increased likelihood of progression to HUS.
Published ahead of print on 13 October 2008.
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