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A Francisella tularensis locus required for spermine responsiveness is necessary for virulence

Brian C Russo1, Joseph Horzempa, Dawn M O'Dee

  • 1Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, 200 Lothrop St., Pittsburgh, PA 15261, USA.

Infection and Immunity
|June 15, 2011
PubMed

Insights

Francisella tularensis uses polyamines for virulence. A specific gene, FTL_0883/FTT_0615c, is crucial for sensing spermine, impacting tularemia pathogenesis and immune evasion.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Tularemia is a severe illness caused by Francisella tularensis, a biodefense agent with broad host range and high mortality.
  • Francisella tularensis interactions with host cells are modulated by polyamines like spermine.
  • Mechanisms of Francisella tularensis environmental sensing and adaptation remain incompletely understood.

Purpose of the Study:

  • To investigate the role of polyamine responsiveness in Francisella tularensis virulence.
  • To identify specific genes involved in Francisella tularensis spermine sensing and their contribution to pathogenesis.

Main Methods:

  • Transposon mutagenesis of Francisella tularensis subsp. holarctica live vaccine strain (LVS) to identify genes involved in spermine response.
  • Construction of in-frame deletion mutants for FTL_0883 (in LVS) and its homologue FTT_0615c (in Francisella tularensis subsp. tularensis Schu S4).
  • In vitro assessment of cytokine production by macrophages and bacterial replication, and in vivo evaluation of virulence in a murine model of pneumonic tularemia.

Main Results:

  • FTL_0883 was identified as a gene critical for spermine responsiveness in F. tularensis.
  • Deletion mutants of FTL_0883 (LVS) and FTT_0615c (Schu S4) induced higher cytokine levels in macrophages.
  • While FTL_0883 deletion attenuated LVS replication in vitro, the Schu S4 FTT_0615c mutant showed similar replication to wild-type.
  • Both LVS and Schu S4 deletion mutants exhibited significant attenuation in vivo, with reduced growth and dissemination of the Schu S4 mutant in a pneumonic tularemia model.
  • The in vivo attenuation was linked to host inflammatory responses.

Conclusions:

  • Responsiveness to polyamines is associated with Francisella tularensis pathogenesis.
  • The FTL_0883/FTT_0615c gene is essential for Francisella tularensis virulence.
  • This gene plays a role in evading the host immune response during tularemia infection.

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