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

Andrew J. Grant, Mark Sheppard, Rob Deardon, Sam P. Brown, Gemma Foster, Clare E. Bryant, Duncan J. Maskell, Pietro Mastroeni

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)28-37
Number of pages10
JournalImmunology
Volume125
Issue number1
DOIs
Publication statusPublished - Sep 2008

Keywords

  • apoptosis
  • caspase
  • necrosis
  • Salmonella typhimurium
  • systemic infection

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