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Infect. Immun. doi:10.1128/IAI.00334-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Inactivation of ibeA and ibeT results in decreased expression of type 1 fimbriae in the Extra-intestinal Pathogenic Escherichia coli strain BEN2908

INRA, UR 1282 Infectiologie Animale et Santé Publique, Laboratoire de Pathogénie Bactérienne, F-37380 Nouzilly, France

^* To whom correspondence should be addressed. Email: Pierre.Germon{at}tours.inra.fr.

	Abstract

IbeA was previously described in Extra-intestinal Pathogenic E. coli (ExPEC) strains for its role in invasion. Here, we investigated the role of IbeA and IbeT, encoded by a gene located downstream of ibeA, in the adhesion of the avian ExPEC strain BEN2908 to Human Brain Microvascular Endothelial Cells (HBMEC). The ibeA mutant was less adhesive to HBMEC than the wild type strain BEN2908. Because strain BEN2908 also expresses type 1 fimbriae, we measured the adhesion specifically due to IbeA by comparing the adhesive properties of a fim derivative of strain BEN2908 to that of a double mutant fim ibeA. No differences were observed indicating that the reduction of adhesion in BEN2908 ibeA could be due to a decrease in type 1 fimbriae expression. We indeed showed that the decreased adhesion of BEN2908 ibeA was correlated with a decrease in type 1 fimbriae expression. Accordingly, more bacteria have a fim promoter orientated in the OFF position in a culture of BEN2908 ibeA than in a culture of BEN2908. Expression of fimB and fimE, two genes encoding recombinases participating in controling the orientation of the fim promoter, was decreased in BEN2908 ibeA. A reduction of type 1 fimbriae expression due to a preferential orientation of the fim promoter in the OFF orientation was also seen in an ibeT mutant of strain BEN2908. We finally suggest a role for IbeA and IbeT in modulating the expression of type 1 fimbriae through an as yet unknown mechanism.