AUGMENTATION BY PLATELETS OF GRANULOCYTE AGGREGATION IN RESPONSE TO CHEMOTAXINS - STUDIES UTILIZING AN IMPROVED CELL PREPARATION TECHNIQUE

  • 1 January 1983
    • journal article
    • research article
    • Vol. 61  (1) , 125-131
Abstract
Considerable evidence exists to suggest roles for both [human] platelets and granulcoytes (PMN) in pulmonary injury in shock. While it was believed that the major contributions of the 2 cell types were sequential, in vitro observations suggested that direct interactions between granulocytes and platelets might also amplify tissue damage. Using isotonic Percoll density gradients to isolate PMN, the effect of deliberate platelet contamination on PMN aggregation was studied. PMN aggregation in response to 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 < 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. 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. Direct as well as sequential platelet/PMN interactions may be important in tissue injury in shock.