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Caspase‐3‐dependent phagocyte death during systemic Salmonella enterica serovar Typhimurium infection of mice
Author(s) -
Grant Andrew J.,
Sheppard Mark,
Deardon Rob,
Brown Sam P.,
Foster Gemma,
Bryant Clare E.,
Maskell Duncan J.,
Mastroeni Pietro
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2008.02814.x
Subject(s) - salmonella enterica , phagocyte , biology , apoptosis , salmonella , microbiology and biotechnology , intracellular parasite , intracellular , programmed cell death , bacteria , macrophage , mononuclear phagocyte system , host (biology) , immunology , phagocytosis , in vitro , genetics
Summary Growth of Salmonella enterica in mammalian tissues results from continuous spread of bacteria to new host cells. Our previous work indicated that infective S. enterica are liberated from host cells via stochastic necrotic burst independently of intracellular bacterial numbers. Here we report that liver phagocytes can undergo apoptotic caspase‐3‐mediated cell death in vivo , with apoptosis being a rare event, more prevalent in heavily infected cells. The density‐dependent apoptotic cell death is likely to constitute an alternative mechanism of bacterial spread as part of a bet‐hedging strategy, ensuring an ongoing protective intracellular environment in which some bacteria can grow and persist.