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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Główni autorzy: Grant, Andrew J, Sheppard, Mark, Deardon, Rob, Brown, Sam P, Foster, Gemma, Bryant, Clare E, Maskell, Duncan J, Mastroeni, Pietro
Format: Artykuł
Język:English
Wydane: Blackwell Science Inc 2008
Hasła przedmiotowe:
Original Articles
Dostęp online: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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Streszczenie: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.

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