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Porcine CD18 mediates Actinobacillus pleuropneumoniae ApxIII species-specific toxicity

Philippe G A C Vanden Bergh1, Laurent L M Zecchinon, Thomas Fett

  • 1Department of Pathology, Faculty of Veterinary Medicine, University of Liege, Liège, Belgium.

Veterinary Research
|April 10, 2009
PubMed

Insights

Actinobacillus pleuropneumoniae

Area of Science:

  • Veterinary Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Actinobacillus pleuropneumoniae causes swine pleuropneumonia, with Apx toxins as key virulence factors.
  • ApxIIIA toxin specifically targets pig leukocytes, similar to toxins affecting human and ruminant leukocytes.
  • LtxA and LktA toxins utilize the CD18 subunit to bind LFA-1 on their respective host cells.

Purpose of the Study:

  • To investigate the role of porcine CD18 in mediating ApxIIIA toxin-induced leukolysis.
  • To determine if ApxIIIA toxin binds to porcine CD18 to exert its cytotoxic effects on leukocytes.

Main Methods:

  • A beta(2)-integrin-deficient, ApxIIIA-resistant human erythroleukemic cell line was used as a recipient.
  • The cell line was transfected with plasmids encoding human, bovine, and porcine CD11a/CD18 heterodimers.
  • Transfected cells were assessed for restored susceptibility to ApxIIIA to identify the critical LFA-1 subunit.

Main Results:

  • The ApxIIIA-resistant cell line became susceptible only when transfected with the porcine CD18 subunit.
  • This indicates that the CD18 partner within the LFA-1 heterodimer is crucial for toxin interaction.
  • Porcine CD18 was identified as the specific binding component for ApxIIIA toxin on leukocytes.

Conclusions:

  • Porcine CD18 is essential for mediating the leukolytic effects of Actinobacillus pleuropneumoniae ApxIIIA toxin.
  • This finding elucidates a specific molecular mechanism of A. pleuropneumoniae virulence in swine.

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