Platelet activation in ponies with airway inflammation

Authors

  • B. Dunkel,

    Corresponding author
    1. Department of Veterinary Basic Sciences, The Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, UK
    Search for more papers by this author
  • K. J. Rickards,

    1. Sackler Institute of Pulmonary Pharmacology, Division of Pharmacology and Therapeutics, GKT School of Biomedical Sciences, King's College London, London Bridge, London SE1 9RT, UK
    Search for more papers by this author
  • C. P. Page,

    1. Sackler Institute of Pulmonary Pharmacology, Division of Pharmacology and Therapeutics, GKT School of Biomedical Sciences, King's College London, London Bridge, London SE1 9RT, UK
    Search for more papers by this author
  • F. M. Cunningham

    1. Department of Veterinary Basic Sciences, The Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, UK
    Search for more papers by this author

Department of Veterinary Basic Sciences, The Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, UK

Summary

Reason for performing study: Platelet activation occurs in human obstructive airway diseases and in laboratory animal models. However, there is limited evidence that platelets may be involved in equine recurrent airway obstruction (RAO) and other inflammatory diseases. This study investigated whether platelet activation also occurred in RAO.

Hypothesis: Platelet function is altered in ponies with active RAO. This alteration can be detected ex vivo by measuring platelet adhesion.

Methods: An in vitro platelet adhesion assay measuring acid phosphatase (AcP) activity colorimetrically was adapted for use with equine platelets and responses to selected agonists were established. Platelet adhesion and aggregation was evaluated in vitro on platelets isolated from 6 ponies with RAO before, during and after a 7 h natural antigen challenge. Three ponies with no history of airway disease were also studied.

Results: Adhesion of equine platelets to serum coated plastic was detected at concentrations of 10–100 times 109/l. Adhesion increased in response to stimulation with platelet activating factor and thrombin, but not equine interleukin 8. Prior to the antigen challenge, adhesion of nonstimulated platelets was low and increased significantly (P<0.05) 24 h after initiation of the challenge in RAOs, but not in the normal animals. No changes in platelet aggregation were noted in either group.

Conclusions: The described assay offers an alternative method to evaluate platelet function in healthy and diseased horses and can detect changes not observed using a classic aggregation assay. Circulating platelets are activated 24 h after antigen challenge of ponies with RAO and may play a role in pulmonary inflammation and/or the pathophysiology of RAO.

Potential relevance: Investigating platelet function in RAO and airway inflammation may reveal new aspects of the pathogenesis of inflammatory lung disease in the horse.

Ancillary