Affiliation:
1. Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University System Health Science Center
2. Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, Texas
Abstract
ABSTRACT
The centisome 63 type III secretion system (T3SS-1) encoded by
Salmonella
pathogenicity island 1 (SPI1) mediates invasion of epithelial cells by
Salmonella enterica
serotype Typhimurium. Characterization of mutants lacking individual genes has revealed that T3SS-1 secreted proteins (effectors) SopE2 and SopB are required for invasion while the SipA protein accelerates entry into cells. Here we have revisited the question of which T3SS-1 effectors contribute to the invasion of epithelial cells by complementing a strain lacking all of the effector genes that are required to cause diarrhea in a calf (a
sipA sopABDE2
mutant). Introduction of either the cloned
sipA
, the cloned
sopB
, or the cloned
sopE2
gene increased the invasiveness of the
sipA sopABDE2
mutant for nonpolarized HT-29 cells. However, a contribution of
sopA
or
sopD
to invasion was not apparent when invasion assays were performed with the nonpolarized colon carcinoma cell lines T84 and HT-29. In contrast, introduction of either the
sopA
, the
sopB
, the
sopD
, or the
sopE2
gene increased the invasiveness of the
sipA sopABDE2
mutant for polarized T84 cells. Furthermore, introduction of a plasmid carrying
sipA
and
sopB
increased the invasiveness of the
sipA sopABDE2
mutant for polarized T84 cells significantly compared to the introduction of plasmids carrying only
sipA
or
sopB
. We conclude that SipA, SopA, SopB, SopD, and SopE2 contribute to
S. enterica
serotype Typhimurium invasion of epithelial cells in vitro.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
256 articles.
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