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Edwardsiella tarda-Induced cytotoxicity depends on its type III secretion system and flagellin

Hai-Xia Xie1, Jin-Fang Lu2, Nathalie Rolhion3

  • 1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China Section of Microbiology, MRC Centre for Molecular Bacteriology and Infection, Imperial College London, London, United Kingdom.

Infection and Immunity
|June 4, 2014
PubMed

Insights

Edwardsiella tarda uses its type III secretion system (T3SS) to infect macrophages, triggering pyroptosis and IL-1β release. Bacteria downregulate FliC to evade host immunity, while hosts detect FliC to control infection.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Gram-negative bacteria employ type III secretion systems (T3SS) to inject virulence factors into host cells, often leading to disease.
  • Macrophages detect secreted bacterial proteins, initiating pyroptosis and releasing proinflammatory cytokines to combat infection.
  • Edwardsiella tarda is an enteric pathogen causing disease in fish and humans.

Purpose of the Study:

  • To investigate the role of the T3SS in E. tarda pathogenesis and host immune response.
  • To elucidate the function of FliC in E. tarda virulence and host immune evasion.

Main Methods:

  • Utilized murine bone marrow-derived macrophages and fish infection models.
  • Generated and analyzed E. tarda mutants with deletions or altered expression of the fliC gene.
  • Assessed macrophage pyroptosis, cytokine secretion (IL-1β), bacterial survival, and virulence.

Main Results:

  • The T3SS of E. tarda is crucial for its survival and replication within macrophages.
  • E. tarda infection induces T3SS-dependent pyroptosis in macrophages from mice and fish, alongside increased IL-1β secretion.
  • Deletion of fliC reduced bacterial cytotoxicity but did not attenuate virulence in fish; overexpressing FliC in a mutant decreased virulence.

Conclusions:

  • The host immune system partially controls E. tarda by detecting FliC translocated via T3SS.
  • E. tarda appears to downregulate FliC expression to evade innate immune detection and promote infection.

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