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Infection and Immunity, November 1998, p. 5580-5586, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Translocated Intimin Receptors (Tir) of
Shiga-Toxigenic Escherichia coli Isolates Belonging to
Serogroups O26, O111, and O157 React with Sera from Patients
with Hemolytic-Uremic Syndrome and Exhibit Marked Sequence
Heterogeneity
Adrienne W.
Paton,1
Paul A.
Manning,2
Matthew C.
Woodrow,1 and
James C.
Paton1,*
Molecular Microbiology Unit, Women's and
Children's Hospital, North Adelaide, South Australia
5006,1 and
Microbial Pathogenesis
Unit, Department of Microbiology and Immunology, University of
Adelaide, Adelaide, South Australia 5005,2
Australia
Received 8 June 1998/Returned for modification 24 July
1998/Accepted 18 August 1998
The capacity to form attaching and effacing (A/E) lesions on the
surfaces of enterocytes is an important virulence trait of several
enteric pathogens, including enteropathogenic Escherichia coli (EPEC) and Shiga-toxigenic E. coli (STEC).
Formation of such lesions depends upon an interaction between a
bacterial outer membrane protein (intimin) and a bacterially encoded
receptor protein (Tir) which is exported from the bacterium and
translocated into the host cell membrane. Intimin, Tir, and several
other proteins necessary for generation of A/E lesions are encoded on a
chromosomal pathogenicity island termed the locus for enterocyte
effacement (LEE). Reports of sequence heterogeneity and antigenic
variation in the region of intimin believed to be responsible for
receptor binding raise the possibility that the receptor itself is also heterogeneous. We have examined this by cloning and sequencing tir genes from three different STEC strains belonging to
serogroups O26, O111, and O157. The deduced amino acid sequences for
the Tir homologues from these strains varied markedly, exhibiting only
65.4, 80.2, and 56.7% identity, respectively, to that recently reported for EPEC Tir. STEC Tir is also highly immunogenic in humans.
Western blots of E. coli DH5
expressing the various STEC tir genes cloned in pBluescript [but not E. coli DH5
(pBluescript)] reacted strongly with convalescent
sera from patients with hemolytic-uremic syndrome (HUS) caused by known
LEE-positive STEC. Moreover, no reaction was seen when the various
clone lysates were probed with serum from a patient with HUS caused by
a LEE-negative STEC or with serum from a healthy individual.
Covariation of exposed epitopes on both intimin and Tir may be a means
whereby STEC avoid host immune responses without compromising
adhesin-receptor interaction.
*
Corresponding author. Mailing address: Molecular
Microbiology Unit, Women's and Children's Hospital, North Adelaide,
S.A. 5006, Australia. Phone: 61-8-8204 6302. Fax: 61-8-8204 6051. E-mail: patonj{at}wch.sa.gov.au.
Infection and Immunity, November 1998, p. 5580-5586, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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