Subcutaneous or intraperitoneal injection of recombinant human granulocyte-macrophage colony-stimulating factor, interleukin 3, or mouse tumour necrosis factor alpha, but not recombinant human interferon gamma, platelet-derived growth factor, or transforming growth factor beta caused selective eosinophilia of the pulmonary airways in the guinea pig. Unlike responses to latelet-activating factor, there was no attendant detectable airway hyperreactivity, but in common with responses to platelet-activating factor, eosinophilia of the airways was prevented by pretreatment with ketotifen or AH 21–132. Cytokines or lymphokines may contribute to pulmonary eosinophilia in diseases such as asthma.
Pharmacological histamine releasing agents, such as compound 48/80, poly-L-lysine, adrenocorticotrophic hormone (ACTH; β 1-24 available commercially as Synacthen®), catecholamines, purine bases, etc., are well known to induce histamine release from rat peritoneal mast cells and mast cells of other species; and to a lesser extent from peripheral blood leucocytes. It is reported in this paper that several of these potent histamine-releasing agents induce little or no histamine release from horse leucocytes. In particular the calcium ionophore A 23187 induced no histamine release. On the other hand concanavalin A induced release of histamine from horse leucocytes, which may be a function of the amount of IgE-like antibodies present on the cells. An anti-horse IgG antiserum presumably reacting with IgE light chains also induced histamine release from horse leucocytes. This antiserum was also used in inhibition studies with isoproterenol, adrenaline and colchicine, which inhibited histamine release in a manner similar to that noted in work on human leucocytes and rat mast cells. The well-known potentiator of histamine release deuterium oxide (D2O) also enhanced histamine release from horse leucocytes in a dose-dependent manner. Although IgE or IgE-like immunoglobulin has not yet been isolated in the equine species, bronchopulmonary allergy in the horse presumably mediated by IgE has been reported. Assessment of histamine release in vitro should permit better comparative studies of this type of allergy.
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