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High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
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Accelerated type III secretion system 2-dependent enteropathogenesis by a Salmonella enterica serovar enteritidis

Mrutyunjay Suar1, Balamurugan Periaswamy, Pascal Songhet

  • 1Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland.

Infection and Immunity
|June 17, 2009
PubMed

Insights

Salmonella Enteritidis and Typhimurium cause enteric disease. This study shows Salmonella Enteritidis uses two pathways, similar to Typhimurium, but triggers inflammation faster via the alternative pathway (TTSS-2).

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Immunology

Background:

  • Salmonella enterica serovars Typhimurium and Enteritidis are significant causes of human enteric illness.
  • The molecular mechanisms of Salmonella Typhimurium pathogenesis, involving type III secretion systems (TTSS-1 and TTSS-2), are well-characterized.
  • The role of these pathways in the pathogenesis of other Salmonella serovars remained unclear.

Purpose of the Study:

  • To investigate the enteropathogenesis of Salmonella Enteritidis PT4/6 (isolate P125109).
  • To determine if the classical (TTSS-1) and alternative (TTSS-2) pathways are involved in Salmonella Enteritidis virulence.
  • To compare the kinetics of inflammation triggered by Salmonella Enteritidis and Salmonella Typhimurium.

Main Methods:

  • Generation of isogenic mutants of Salmonella Enteritidis P125109.
  • In vitro and in vivo infection models.
  • Dendritic cell depletion and MyD88 knockout mouse studies.

Main Results:

  • Salmonella Enteritidis P125109 utilizes both TTSS-1 and TTSS-2 pathways to induce mucosal inflammation.
  • The classical pathway function was comparable between Salmonella Enteritidis and Salmonella Typhimurium.
  • The alternative pathway (TTSS-2) in Salmonella Enteritidis mediated faster gut colonization and inflammation induction compared to Salmonella Typhimurium.

Conclusions:

  • Both classical and alternative pathways contribute to Salmonella Enteritidis enteropathogenesis.
  • Salmonella species exhibit differential kinetics in triggering mucosal inflammation via the alternative pathway (TTSS-2).
  • These findings highlight serovar-specific variations in Salmonella virulence mechanisms.

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