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Virulence plasmid of Aeromonas hydrophila induces macrophage apoptosis and helps in developing systemic infection in

Tanmay Majumdar1, Pritam Chattopadhyay, Dhira Rani Saha

  • 1Immunobiology Laboratory, School of Life Sciences, Visva-Bharati University, Santiniketan 731 235, India.

Microbial Pathogenesis
|December 2, 2008
PubMed

Insights

The 21kb plasmid in Aeromonas hydrophila AO1 is a key virulence factor. It suppresses IL-1beta and induces macrophage apoptosis, enabling systemic infection in mice.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Pathogenic Aeromonas hydrophila strains possess virulence factors that contribute to disease.
  • Understanding the genetic basis of virulence is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of a 21kb plasmid in the virulence of Aeromonas hydrophila strain AO1.
  • To elucidate the mechanisms by which this plasmid contributes to pathogenesis in a murine model.

Main Methods:

  • Plasmid curing and transformation experiments in Aeromonas hydrophila.
  • In vitro studies on macrophage cytotoxicity and apoptosis assays (Hoechst 33342, Annexin-V, TUNEL).
  • In vivo infection studies in BALB/c mice, including bacterial load assessment and cytokine analysis (ELISA for IL-1beta).

Main Results:

  • The 21kb plasmid confers cytotoxicity and induces apoptosis in BALB/c mice splenic macrophages via caspase pathways.
  • Plasmid-bearing isolates suppressed pro-inflammatory cytokine IL-1beta production.
  • Curing the plasmid reduced virulence, while re-transformation restored it, confirming the plasmid's role.
  • Plasmid-cured isolates were cleared more rapidly by the host immune system.

Conclusions:

  • The 21kb plasmid is a critical virulence factor for Aeromonas hydrophila AO1 in mice.
  • It facilitates immune evasion by inducing macrophage apoptosis and suppressing IL-1beta, leading to systemic infection.

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