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Cytotoxic interactions between bovine parainfluenza type 3 virus and bovine alveolar macrophages

B M Adair1, H E Bradford, M S McNulty

  • 1Veterinary Sciences Division, Belfast, Ireland. brian.adair@dani.gov.uk

Insights

Bovine alveolar macrophages kill parainfluenza type 3 virus-infected cells independently of antibodies. Cytotoxicity increases after infection but is regulated by extracellular factors in lung lavage fluids.

Area of Science:

  • Veterinary Immunology
  • Cellular Immunology
  • Virology

Background:

  • Bovine alveolar macrophages play a role in lung immunity.
  • Parainfluenza type 3 (PI-3) virus is a significant respiratory pathogen in cattle.

Purpose of the Study:

  • To investigate the cytotoxic activity of bovine alveolar macrophages against PI-3 virus-infected cells.
  • To determine the role of antibodies and extracellular factors in this cytotoxicity.

Main Methods:

  • 51Cr release assays were used to measure cytotoxic activity.
  • Macrophage cytotoxicity was assessed in vitro and in vivo following PI-3 virus infection in calves.
  • Extracellular factors in lavage fluids were analyzed for their effect on cytotoxicity.

Main Results:

  • Bovine alveolar macrophages exhibited antibody-independent cell-mediated cytotoxicity against PI-3 virus-infected cells.
  • Cytotoxicity levels varied significantly between individual animals.
  • PI-3 virus antiserum inhibited, rather than enhanced, macrophage cytotoxicity.
  • Macrophage cytotoxicity increased substantially after PI-3 virus inoculation in vivo, peaking by Day 5.
  • Extracellular factors in lung lavage fluids largely controlled macrophage cytotoxic activity.

Conclusions:

  • Bovine alveolar macrophages possess intrinsic cytotoxic capabilities against PI-3 virus-infected cells.
  • Antibody-dependent cytotoxicity is not consistently observed and can be inhibited by antiserum.
  • Extracellular factors present in the lung environment significantly modulate macrophage cytotoxic function.

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