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Caspase-3-dependent phagocyte death during systemic Salmonella enterica serovar Typhimurium infection of mice

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 li...

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Detalhes bibliográficos
Main Authors: Grant, Andrew J, Sheppard, Mark, Deardon, Rob, Brown, Sam P, Foster, Gemma, Bryant, Clare E, Maskell, Duncan J, Mastroeni, Pietro
Formato: Artigo
Idioma:English
Publicado em: Blackwell Science Inc 2008
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Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2526257/
https://ncbi.nlm.nih.gov/pubmed/18298550
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1365-2567.2008.02814.x
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Resumo: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.