No abstract

The uptake of the monoamine radiolabelled tracer 125I-meta-iodo-benzyl-guanidine (MIBG) was studied in vitro in platelets from 15 healthy volunteers and five allergic patients whose serum IgE concentration was 37 +/- 33 and 650 +/- 200 IU/ml, respectively. The MIBG uptake was determined by means of a gamma counter after incubation in a buffer. Binding of IgE to platelets significantly reduced MIBG uptake both in healthy subjects and in allergic patients. This reduction was significantly related to the action of IgE as it did not occur after binding of IgG. Moreover, MIBG uptake plotted versus increasing concentration of IgE (ranging from 10 to 3000 IU/ml) was fitted by a classical sigmoidal curve which was not significantly different between healthy subjects and allergic patients. Lastly, the effect of IgE on MIBG uptake was due to the binding of the sole IgE as it was not modified by subsequent addition of anti-IgE. It is concluded that the binding of the sole IgE to its specific receptor on platelets alters the transport of monoamines.

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.