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Thoughts on mast cells, histamine release and immunoglobulin E.
International Archives of Allergy and Applied Immunology
|January 1, 1985
Summary
Dextran and acetylcholine trigger histamine release from rat mast cells, with IgE antibodies significantly enhancing this response. This study explores the physiological and pathological roles of these mediators in histamine secretion.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Dextran polysaccharide is known to stimulate histamine secretion from rat mast cells, likely via interaction with cell-fixed immunoglobulin E (IgE).
- Passive sensitization with antigens enhances dextran-induced histamine release, which is abolished by removing IgE using acidic pH.
- IgE antibodies play a crucial role in histamine release from mast cells induced by various agents, not just dextran.
Purpose of the Study:
- To investigate the mechanisms of histamine release from mast cells.
- To explore the role of immunoglobulin E (IgE) in mast cell activation.
- To examine the involvement of cholinergic agents and substance P in histamine secretion.
Main Methods:
- In vitro experiments using rat mast cells.
- Histamine release assays.
- Modulation of IgE levels on mast cells.
Main Results:
- Dextran stimulates histamine secretion, potentiated by IgE.
- Acetylcholine induces non-immunological histamine release, also potentiated by IgE.
- A potential link between cholinergic agents and substance P in histamine release is suggested.
Conclusions:
- Immunoglobulin E (IgE) is critical for dextran-induced histamine release and potentiates acetylcholine-induced release.
- Histamine release mechanisms involve both IgE-dependent and independent pathways.
- Further research is needed to elucidate the interplay between cholinergic signaling, substance P, and mast cell activation.