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Mouse infection by Legionella, a model to analyze autophagy

Journal

AUTOPHAGY
Volume 2, Issue 3, Pages 179-182

Publisher

LANDES BIOSCIENCE
DOI: 10.4161/auto.2831

Keywords

intracellular pathogen; flagellin; inflammasome; NLR; Naip5; caspase-1; programmed cell death; innate immunity

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Funding

  1. NIAID NIH HHS [R01 AI040694, R01 AI040694-06AI] Funding Source: Medline

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Autophagy is a conserved membrane traffic pathway that equips eukaryotic cells to capture cytoplasmic components within a double-membrane vacuole, or autophagosome, for delivery to lysosomes. Although best known as a mechanism to survive starvation, autophagy is now recognized to combat infection by a variety of microbes.(1-3) Not surprisingly, to establish a replication niche in host cells, some intracellular pathogens have acquired mechanisms either to evade or subvert the autophagic pathway. Because they are amenable to genetic manipulation, these microbes can be exploited as experimental tools to investigate the contribution of autophagy to immunity. Here we discuss the mouse macrophage response to L. pneumophila, the facultative intracellular bacterium responsible for an acute form of pneumonia, Legionnaire's disease.

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