Modulation of the immunological release of the eosinophil chemotactic factor of anaphylaxis from human lung.

The antigen-induced release of preformed eosinophil chemotactic factor of anaphylaxis (ECF-A) from passively sensitized human lung tissue, requires divalent cations, an intact glycolytic pathway and a diisopropyl fluorophosphate (DFP) inhibitable esterase, and appears to be modulated by prototype adrenergic and cholinergic receptors. Increases in intracellular cyclic AMP inhibit the release of ECF-A as shown not only by the effect of exogenous dibutyryl cyclic AMP but also by the kinetic relationship between increases in tissue cyclic AMP and inhibition of the release of ECF-A, histamine and slow reacting substance of anaphylaxis from lung tissue interacted with cholera toxin. Cholinergic enhancement of the antigen-induced release of ECF-A was not associated with measurable alterations in the intracellular content of cyclic AMP and is attributed to elevation of intracellular cyclic GMP, as the introduction of 8-bromo cyclic GMP enhances ECF-A release.