With the rosette technique, the ECF-A tetrapeptides (Val-Gly-Ser-Glu and Ala-Gly-Ser-Glu) and histamine, agents previously shown to be preferentially chemotactic for the eosinophil, markedly enhanced the expression of human eosinophil receptors for C3b. The enhancement was both dose- and time-dependent, and highly selective for the eosinophil since there was no evidence that C3b receptors on neutrophils or monocytes were altered by these pharmacologic agents even when varying concentrations of C3 were added to the indicator red cells. The agents similarly enhanced receptors for C4, but under the same conditions C3d and IgG (Fc) receptors were unaffected.
A number of other pharmacologic mediators including bradykinin and the prostaglandins PGE1, E2, and F2α had no apparent effect on eosinophil C3b receptors at the same molar concentrations (5 × 10-5 to 5 × 10-7 moles 1-1). However, a major histamine catabolite, imidazoleacetic acid, also recognized as an anaphylaxis-associated eosinophilotactic agent, enhanced eosinophil C3b receptors to a degree comparable to that of histamine. In contrast, l-histidine and the histamine catabolites, N-acetylhistamine, 1,4-methylhistamine, and 1-methyl-4-imidazoleacetic acid, had no eosinophil C3b receptor-enhancing effect. 5-hydroxytryptamine at the highest concentration tested (5 × 10-5 moles 1-1) gave enhancment of eosinophil C3b receptors which was approximately one-third of that achieved with the same concentration of the ECF-A peptides, histamine, or imidazoleacetic acid.
A human lung anaphylactic diffusate also enhanced eosinophil C3b receptors. Approximately 10 times more synthetic histamine than that contained in the lung-derived material was required for comparable enhancement, indicating that the histamine and ECF-A peptides present in the diffusate may have combined to give optimal enhancing effect. However, when synthetic histamine and the valyl- or alanyl-peptide, were mixed in various proportions, the enhancement was no greater than that achieved when each agent was tested alone.
These results suggest that pharmacologic mediators of hypersensitivity may regulate certain eosinophil-dependent biologic reactions and that there may be a direct relationship between the cell surface “recognition unit” for eosinophil locomotion and some of the membrane receptors that promote the adhesion of eosinophils to opsonized particles.