Journal
AUTOPHAGY
Volume 1, Issue 3, Pages 174-176Publisher
LANDES BIOSCIENCE
DOI: 10.4161/auto.1.3.2067
Keywords
pyroptosis; caspase 1; IL-1; inflammasome; NOD protein; Naip5; macrophages; Legionella pneumophilia
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Funding
- NIAID NIH HHS [R01 AI040694] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007544] Funding Source: Medline
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By low in the evolutionary jungle, any host defense mechanism that efficiently kills microbes also exerts a strong selective pressure for tolerant variants to emerge. As a consequence, pathogens can be exploited as powerful tools to examine host defense mechanisms. Recent studies of the confrontation between macrophages and the opportunistic pathogen Legionella pneumophila have revealed a regulatory mechanism that may link autophagy to pyroptosis, a type of programmed cell death. Building from the extensive literature on autophagy, cell death, and innate immunity, we propose here a testable model in which the NOD-LRR protein Naip5 dictates whether murine macrophages elevate autophagy or pyroptosis as a barrier to infection.
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