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Caspase Exploitation by Legionella pneumophila

Kathrin Krause1, Amal O Amer1

  • 1Department of Microbial Infection and Immunity, The Ohio State University Columbus, OH, USA.

Frontiers in Microbiology
|May 6, 2016
PubMed

Insights

Legionella pneumophila evades inflammasome activation in human macrophages but triggers bacterial restriction in mouse cells. This difference highlights host cell-specific immune responses to Legionella infection.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Legionella pneumophila is a significant pathogen, particularly affecting hospitalized individuals.
  • The bacterium can survive extracellularly or within amoebae in the environment.
  • L. pneumophila infects alveolar macrophages in humans, evading inflammasome activation and caspase-1 cleavage.

Purpose of the Study:

  • To review current knowledge on inflammasome pathways activated by L. pneumophila.
  • To compare host cell responses in permissive (human) and restrictive (murine) macrophages.
  • To elucidate mechanisms of bacterial recognition and host defense against L. pneumophila.

Main Methods:

  • Review of existing literature on L. pneumophila-host cell interactions.
  • Analysis of inflammasome signaling pathways (canonical and non-canonical).
  • Comparison of immune responses in human alveolar macrophages versus murine macrophages.

Main Results:

  • Human macrophages permit L. pneumophila replication without inflammasome activation.
  • Murine macrophages recognize intracellular L. pneumophila, initiating inflammasome-mediated responses.
  • These murine responses include cytokine secretion, phagosomal maturation, and pyroptotic cell death, restricting bacterial growth.

Conclusions:

  • Host cell type dictates the outcome of L. pneumophila infection, specifically regarding inflammasome activation.
  • Flagellin-dependent and -independent pathways are involved in triggering inflammasomes in response to L. pneumophila.
  • Understanding these differential host responses is crucial for developing therapeutic strategies against Legionnaires' disease.
Keywords:
Legionella pneumophilaNOD like receptorscaspasescell death mechanismsphagosomal maturation

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