Augmentation by platelets of granulocyte aggregation in response to chemotaxins: studies utilizing an improved cell preparation technique.
Considerable evidence exists to suggest roles for both platelets and granulocytes (PMNs) in pulmonary injury in shock. While believing that the major contributions of the two cell types are sequential, in vitro observations suggested that direct interactions between granulocytes and platelets might also amplify tissue damage. Using isotonic Percoll density gradients to isolate PMNs, we therefore studied the effect of deliberate platelet contamination on PMN aggregation. PMN aggregation in response to N-formyl-met-leu-phe or activated complement was enhanced by the presence of 1 platelet/PMN, an effect that became maximal at 16 platelets/PMN (p less than 0.01); large mixed aggregates were formed. Lysed, aspirinated, and indomethacin-treated platelets retained their augmentative capacity, as did platelets washed by gel filtration. The effect was not mimicked by the addition of histamine or serotonin to PMN preparations. None of these platelet preparations augmented lysosomal enzyme release. We conclude that platelets augment PMN aggregation, both by forming giant mixed PMN/platelet aggregates and also by producing a labile augmentative substance, the production of which may be independent of thromboxane synthesis. We propose that direct as well as sequential platelet/PMN interactions may be important in tissue injury in shock.
D001792:Blood Platelets / Q000502:physiology*; D002449:Cell Aggregation; D002450:Cell Communication; D002469:Cell Separation / Q000379:methods*; D002630:Chemotactic Factors / Q000502:physiology*; D006098:Granulocytes / Q000502:physiology; D006801:Humans; D009504:Neutrophils / Q000166:cytology*; D012128:Respiratory Distress Syndrome / Q000097:blood
D002630:Chemotactic Factors