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Updated: Jan 8, 2026
Humanized Mediator Release Assay as a Read-Out for Allergen Potency
Published on: June 29, 2021
Interleukin 1 releases histamine from human basophils and mast cells in vitro
Interleukin (IL 1) preparations from five different sources (human monocyte, LPS-stimulated, purified IL 1 from two different laboratories) and human recombinant IL 1 (HrIL 1) were shown to be capable of directly inducing histamine (HA) release from human basophils (10 to 50% of total cellular HA, depending on the source of IL 1). The release was not due to the medium, pyrogens, or other contaminants. Il 1-induced HA release was dose dependent between 1 to 100 U/ml of IL 1 and 1 to 15 ng/ml of HrIL 1 and was rapid, with a peak release at 15 min. HA release induced by IL 1 was blocked completely by preexposure of cells to IL 1 but was not affected by prechallenge with anti-IgE. Also, preincubation of IL 1 with anti-IL 1 antibody abolished the HA-releasing activity. IL 1-induced HA release was also observed in preparations of human adenoidal mast cells. Our data indicate that it is unlikely that the HA release induced by IL 1 is due to a contamination with HA-releasing factor. This effect of IL 1 provides a mechanism for non-IgE-related local HA release and raises the possibility of a link between cellular immunity and immediate hypersensitivity of potential importance for the pathology of immuno/inflammatory diseases.
Interleukin (IL 1) preparations from five different sources (human monocyte, LPS-stimulated, purified IL 1 from two different laboratories) and human recombinant IL 1 (HrIL 1) were shown to be capable of directly inducing histamine (HA) release from human basophils (10 to 50% of total cellular HA, depending on the source of IL 1). The release was not due to the medium, pyrogens, or other contaminants. Il 1-induced HA release was dose dependent between 1 to 100 U/ml of IL 1 and 1 to 15 ng/ml of HrIL 1 and was rapid, with a peak release at 15 min. HA release induced by IL 1 was blocked completely by preexposure of cells to IL 1 but was not affected by prechallenge with anti-IgE. Also, preincubation of IL 1 with anti-IL 1 antibody abolished the HA-releasing activity. IL 1-induced HA release was also observed in preparations of human adenoidal mast cells. Our data indicate that it is unlikely that the HA release induced by IL 1 is due to a contamination with HA-releasing factor. This effect of IL 1 provides a mechanism for non-IgE-related local HA release and raises the possibility of a link between cellular immunity and immediate hypersensitivity of potential importance for the pathology of immuno/inflammatory diseases.
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