Open AccessSalmonella enterica Replication in Hemophagocytic Macrophages Requires Two Type Three Secretion Systems
Author(s) -
Eugenia Silva-Herzog,
Corrella S. Detweiler
Publication year - 2010
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00292-10
Subject(s) - salmonella enterica , biology , microbiology and biotechnology , salmonella , type three secretion system , enterobacteriaceae , secretion , bacteria , escherichia coli , multidrug tolerance , macrophage , multiplicity of infection , virology , virulence , virus , in vitro , biofilm , gene , biochemistry , genetics
Salmonella enterica serotype Typhimurium is a natural pathogen of mice, which acquire the bacteria orally and develop systemic acute infections that can become subacute to chronic infections.S. Typhimurium can reside within hemophagocytic macrophages (HMs) in SV129S6 mice, an Slc11a1/Nramp1+/+ inbred strain. HMs are activated macrophages which have ingested viable hematopoietic cells and are a key characteristic of infectious and inflammatory diseases. Here we show that modestS. Typhimurium replication in HMs begins at 18 h postinfection, while activated macrophages kill the bacteria. For bacterial replication to occur, the phagocytosed viable cells must be grown to a low cell density and the multiplicity of infection must be low. HMs are able to kill phagocytosedEscherichia coli , produce reactive nitrogen species, and retainS. Typhimurium within membrane-bound vesicles.S. Typhimurium does not rescueE. coli upon coinfection of HMs. This indicates thatS. Typhimurium does not cause HMs to become permissive for other microbes; rather,S. Typhimurium is especially equipped to survive within HMs. Two type three secretion systems (T3SS) encoded byS. Typhimurium are required for replication within HMs. While the T3SS withinSalmonella pathogenicity island 2 (SPI-2) has been previously shown to be important for bacterial survival in cells, a role for SPI-1 in replication in macrophages has not been reported. The requirement for SPI-1 in HMs may help explain the role of SPI-1 during long-term colonization of mice.