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Infection and Immunity, February 1999, p. 490-495, Vol. 67, No. 2
Biotechnology Laboratory and Departments of
Microbiology & Immunology and of Biochemistry & Molecular
Biology, University of British Columbia, Vancouver, British Columbia
V6T 1Z3, Canada
Received 16 March 1998/Returned for modification 27 May
1998/Accepted 24 November 1998
Enteropathogenic Escherichia coli (EPEC) interacts with
intestinal epithelial cells, activating host signaling pathways leading to cytoskeletal rearrangements and ultimately diarrhea. In this study,
we demonstrate that EPEC interacts with the macrophage-like cell line
J774A.1 to inhibit phagocytosis by these cells. Antiphagocytic activity
was also observed in cultured RAW macrophage-like cells upon EPEC
infection. The EPEC antiphagocytic phenotype was dependent on the type
III secretion pathway of EPEC and its secreted proteins, including
EspA, EspB, and EspD. Intimin and Tir mutants displayed intermediate
antiphagocytic activity, suggesting that intimate attachment mediated
by intimin-Tir binding may also play a role in antiphagocytosis.
Tyrosine dephosphorylation of several host proteins was observed
following infection with secretion-competent EPEC but not with
secretion-deficient mutants. Dephosphorylation was detectable 120 min
after infection with EPEC, directly correlating with the onset of the
antiphagocytic phenotype. Inhibition of protein tyrosine phosphatases
by pervanadate treatment increased the number of intracellular
wild-type EPEC organisms to levels seen with secretion-deficient
mutants, suggesting that dephosphorylation events are linked to the
antiphagocytic phenotype. No tyrosine phosphatase activity was detected
with the EPEC-secreted proteins, suggesting that EPEC induces
antiphagocytosis via a different mechanism than Yersinia
species. Taken together, the present findings demonstrate a novel
function for EPEC-secreted proteins in triggering macrophage protein
tyrosine dephosphorylation and inhibition of phagocytosis.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Enteropathogenic Escherichia coli
Inhibits Phagocytosis
and
*
Corresponding author. Mailing address: Biotechnology
Laboratory and Departments of Microbiology & Immunology and of
Biochemistry & Molecular Biology, University of British Columbia,
Vancouver, British Columbia V6T 1Z3, Canada. Phone: (604) 822-2210. Fax: (604) 822-9830. E-mail: bfinlay{at}unixg.ubc.ca.
Present address: Department of Pathology and Microbiology, School
of Medical Sciences, University of Bristol, Bristol BS8 1TD, Great Britain.
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