Affiliation:
1. Department of Microbiology and Immunology, University of Kentucky Chandler Medical Center, Lexington, Kentucky 40536-0084
2. Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, Illinois 60611
Abstract
ABSTRACT
We have previously shown that
Legionella pneumophila
induces caspase 3-dependent apoptosis in mammalian cells during early stages of infection. In this report, we show that nine
L. pneumophila
strains with mutations in the
dotA
,
dotDCB
,
icmT
,
icmGCD,
and
icmJB
loci are completely defective in the induction of apoptosis, in addition to their severe defects in intracellular replication and pore formation-mediated cytotoxicity. Importantly, all nine
dot
/
icm
mutants were complemented for all their defective phenotypes with the respective wild-type loci. We show that the role of the Dot/Icm type IV secretion system in the induction of apoptosis is independent of the RtxA toxin, the
dot
/
icm
-regulated pore-forming toxin, and the type II secretion system. However, the pore-forming toxin, which is triggered upon entry into the postexponential growth phase, enhances the ability of
L. pneumophila
to induce apoptosis. Our data provide the first example of the role of a type IV secretion system of a bacterial pathogen in the induction of apoptosis in the host cell.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
107 articles.
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