Affiliation:
1. Departments of Microbiology
2. Medicine
3. Genome Sciences, University of Washington, Seattle, Washington 98195
Abstract
ABSTRACT
The
Salmonella enterica
serovar Typhimurium type III secretion system (TTSS) encoded in
Salmonella
pathogenicity island 2 (SPI-2) promotes replication within host cells and systemic infection of mice. The SPI-2 TTSS is expressed following
Salmonella
internalization into host cells and translocates effectors across the membrane of the
Salmonella
-containing vacuole (SCV). Two effectors with similar amino-terminal domains, SseJ and SifB, localize to the SCV membrane in infected HEp-2 cells and subsequently traffic away from the SCV along
Salmonella-
induced-filaments (Sifs). Following infection of RAW cells, SseJ and SifB localize to the SCV as well as LAMP-1-positive, vesicular-appearing structures distant from the SCV. Trafficking of SseJ and SifB away from the SCV requires the SPI-2 effector SifA. Deletion of
sseJ
, but not
sifB
, leads to attenuation of
Salmonella
replication in mice following intraperitoneal inoculation. The contribution of SseJ to in vivo replication is identical in wild-type and
sifA
deletion backgrounds, suggesting that SseJ trafficking away from the SCV along Sifs is unnecessary for its virulence function.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
123 articles.
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