Letter | Published:

Release of Serotonin from Human Platelets in Hypersensitivity States

Naturevolume 214pages286287 (1967) | Download Citation



THAT histamine may be released from platelets both in vivo and in vitro in sensitized animals and in man during the course of antigen–antibody reactions has been known for some time, and attempts have been made to use this phenomenon for the in vitro diagnosis of clinical hypersensitivity states4. The liberation of serotonin as well as histamine from platelets by antigen–antibody reactions was described in detail by Humphrey and Jaques1 using platelets from several species including man. These workers used sera from rabbits immunized with either pneumococcus polysaccharide or ovalbumin and concluded that the release reaction required calcium ions and plasma or serum for maximal activity. Heating the plasma or serum to 56° C reduced the amount of serotonin or histamine released. Similar results were obtained by in vivo studies of anaphylaxis in the rabbit showing an increase in the plasma histamine and serotonin levels following challenge accompanied by a fall in the number of circulating platelets6,7. The aggregation of platelets by antigen–antibody complexes was described by Miescher and Cooper2 and also by Siqueira and Nelson5 as probably being caused by the combination of the complexes with one of the components of complement and this final complex binding on the platelet surface. More recently Movat, Mustard, Taichman and Uriuhara3 were able to show platelet aggregation and adenosine diphosphate (ADP) release as well as liberation of histamine and serotonin by the action of rabbit bovine serum albumin—anti-bovine serum albumin and ferritin—anti-ferritin complexes on human or pig platelets. They suggest that phagocytosis of the antigen–antibody complex releases ADP which causes aggregation and in turn releases serotonin, histamine and further ADP.

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  1. 1

    Humphrey, J. H., and Jaques, R., J. Physiol., 128, 9 (1955).

  2. 2

    Miescher, P., and Cooper, N., Vox Sang., 5, 138 (1960).

  3. 3

    Movat, H. Z., Mustard, J. F., Taichman, N. S., and Uriuhara, T., Proc. Soc. Exp. Biol. and Med., 120, 232 (1965).

  4. 4

    Shelley, W. B., and Comaish, J. S., J. Amer. Med. Assoc., 192, 36 (1965).

  5. 5

    Siqueira, M., and Nelson, R. A., J. Immunol., 86, 516 (1961).

  6. 6

    Waalkes, T. P., Weissbach, H., Bozicevich, J., and Udenfriend, S., J. Clin. Invest., 36, 1115 (1957).

  7. 7

    Waalkes, T. P., Weissbach, H., Bozicevich, J., and Udenfriend, S., Proc. Soc. Exp. Biol. and Med., 95, 479 (1957).

  8. 8

    de Weck, A. L., Nature, 202, 975 (1964).

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  1. M.R.C. Demyelinating Diseases Research Unit

    • E. A. CASPARY
  2. Department of Dermatology, University of Newcastle upon Tyne

    • J. S. COMAISH


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