Listeria monocytogenes and Shigella flexneri Activate the NLRP1B Inflammasome

Infect Immun. 2017 Oct 18;85(11):e00338-17. doi: 10.1128/IAI.00338-17. Print 2017 Nov.


Activation of the innate immune receptor NLRP1B leads to the formation of an inflammasome, which induces autoproteolytic processing of pro-caspase-1, and ultimately to the release of inflammatory cytokines and to the execution of pyroptosis. One of the signals to which NLRP1B responds is metabolic stress that occurs in cells deprived of glucose or treated with metabolic inhibitors. NLRP1B might therefore sense microbial infection, as intracellular pathogens such as Listeria monocytogenes and Shigella flexneri cause metabolic stress as a result of nutrient scavenging and host cell damage. Here we addressed whether these pathogens activate the NLRP1B inflammasome. We found that Listeria infection activated the NLRP1B inflammasome in a reconstituted fibroblast model. Activation of NLRP1B by Listeria was diminished in an NLRP1B mutant shown previously to be defective at detecting energy stress and was dependent on the expression of listeriolysin O (LLO), a protein required for vacuolar escape. Infections of either Listeria or Shigella activated NLRP1B in the RAW264.7 murine macrophage line, which expresses endogenous NLRP1B. We conclude that NLRP1B senses cellular infection by distinct invasive pathogens.

Keywords: Listeria monocytogenes; NLRP1B; Shigella; caspase-1; inflammasome.

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins / deficiency
  • Apoptosis Regulatory Proteins / genetics*
  • Apoptosis Regulatory Proteins / immunology
  • Bacterial Toxins / genetics*
  • Bacterial Toxins / metabolism
  • Cell Line
  • Cell Line, Tumor
  • Fibroblasts / immunology
  • Fibroblasts / microbiology
  • Gene Expression Regulation
  • Heat-Shock Proteins / genetics*
  • Heat-Shock Proteins / metabolism
  • Hemolysin Proteins / genetics*
  • Hemolysin Proteins / metabolism
  • Host-Pathogen Interactions
  • Humans
  • Inflammasomes / genetics*
  • Inflammasomes / immunology
  • Listeria monocytogenes / genetics*
  • Listeria monocytogenes / growth & development
  • Listeria monocytogenes / metabolism
  • Macrophages / immunology
  • Macrophages / microbiology
  • Mice
  • Mutation
  • Shigella flexneri / genetics*
  • Shigella flexneri / growth & development
  • Shigella flexneri / metabolism
  • Signal Transduction


  • Apoptosis Regulatory Proteins
  • Bacterial Toxins
  • Heat-Shock Proteins
  • Hemolysin Proteins
  • Inflammasomes
  • Nalp1b protein, mouse
  • hlyA protein, Listeria monocytogenes

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