IgE binding inhibits arachidonic acid-induced chemiluminescence of human platelets

Arachidonic acid (AA)-induced chemiluminescence (CHL) was studied in vitro by means of a luminometer in platelets from nine healthy volunteers and six allergic patients. The amplitude of the CHL signal increased with AA concentration from 250 microM to 7 mM. At a low AA concentration (250 microM), the CHL signal consisted of two peaks. The first one occurred at 6 +/- 3 sec and the second one at 90 +/- 15 sec (n = 9). The mean amplitude of these peaks was 1.95 +/- 0.61 mV/sec and 0.82 +/- 0.22 mV/sec for normal subjects, and 2.35 +/- 0.62 mV/sec and 0.78 +/- 0.26 mV/sec for allergic patients, respectively. Aspirin (a cyclooxygenase inhibitor) and baicalein (a lipoxygenase inhibitor) reduced in a concentration-dependent manner, the first and second peak, respectively. The binding of immunoglobulin E (IgE) alone to platelets from both normal and allergic subjects inhibited both the first and second peak of AA-induced CHL. This inhibitory effect was specifically due to the action of IgE as it was (i) concentration-dependent and (ii) not observed when immunoglobulin G (IgG) was substituted for IgE. It is concluded that in normal subjects, as well as in allergic patients, the binding of IgE alone to its specific receptor on human platelets could alter arachidonate metabolism that probably involves cyclooxygenase and lipoxygenase pathways.