Regulatory role of prostaglandin E in allergic histamine release with observations on the responsiveness of basophil leukocytes and the effect of acetylsalicylic acid

Abstract

This study examined the relationship between prostaglandin E (PGE) production and antigen-induced histamine release by leukocytes of asthmatic patients. The maximum amount of antigen-induced histamine release from leukocytes of different donors did not correlate with serum ragweed-specific IgE levels and correlated inversely with the basal PGE release from cultured leukocytes. The relationship betwen maximum histamine release and serum ragweed-specific IgE levels appeared to be influenced by the degree of PGE release. Patients with lower histamine release relative to ragweed-specific IgE levels had elevated PGE release. Based on these findings it can be hypothesized that spontaneously produced PGE might be a determinant of the responsiveness of basophil leukocytes to immunologic stimulation. This hypothesis was supported by demonstration of a positive correlation between the degree of inhibition of total basal PGE production in leukocyte suspensions during a short period of incubation and the degree of enhancement of antigen-induced histamine release by acetylsalicylic acid (ASA). The results indicate that, although the presence of IgE antibody in the blood may be the prerequisite for allergic histamine release from human leukocytes, endogenous PGE may be an important regulator of the release reaction. The results also suggest that idiosyncratic reactions to ASA and other nonsteroidal anti-inflammatory drugs observed in the allergic population may be at least partly due to impairment of the regulator function of endogenous PGE in the IgE-mediated histamine release reaction.