Inflammasome-mediated cell death in response to bacterial pathogens that access the host cell cytosol: lessons from legionella pneumophila

Front Cell Infect Microbiol. 2013 Dec 27;3:111. doi: 10.3389/fcimb.2013.00111.

Abstract

Cell death can be critical for host defense against intracellular pathogens because it eliminates a crucial replicative niche, and pro-inflammatory cell death can alert neighboring cells to the presence of pathogenic organisms and enhance downstream immune responses. Pyroptosis is a pro-inflammatory form of cell death triggered by the inflammasome, a multi-protein complex that assembles in the cytosol to activate caspase-1. Inflammasome activation by pathogens hinges upon violation of the host cell cytosol by activities such as the use of pore-forming toxins, the use of specialized secretion systems, or the cytosolic presence of the pathogen itself. Recently, a non-canonical inflammasome has been described that activates caspase-11 and also leads to pro-inflammatory cell death. Caspase-11 is activated rapidly and robustly in response to violation of the cytosol by bacterial pathogens as well. In this mini-review, we describe the canonical and non-canonical inflammasome pathways that are critical for host defense against a model intracellular bacterial pathogen that accesses the host cytosol-Legionella pneumophila.

Keywords: Legionella pneumophila; caspase-1; caspase-11; cell death; inflammasome; pyroptosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Caspases / immunology
  • Caspases / metabolism*
  • Cell Death*
  • Cytosol / microbiology*
  • Inflammasomes / immunology
  • Inflammasomes / metabolism*
  • Legionella pneumophila / immunology*
  • Legionnaires' Disease / immunology*
  • Legionnaires' Disease / microbiology*

Substances

  • Inflammasomes
  • Caspases