Mast cell histamine release inhibition

“Mast cell histamine release inhibition” refers broadly to any mechanism or intervention that prevents or reduces the exocytosis-mediated secretion of preformed granule-stored mediators—primarily histamine—from activated mast cells. This biological effect can be achieved through various pharmacologic agents known as “mast-cell stabilizers” such as cromolyn sodium and nedocromil sodium; these act by interfering with intracellular signaling pathways essential for degranulation—including calcium influx and calmodulin activity—or by increasing cyclic AMP within the cells. Many anti-allergic drugs exploit these mechanisms to treat diseases characterized by inappropriate or excessive activation of tissue-resident mast cells such as asthma, allergic rhinitis, urticaria, atopic dermatitis, and anaphylaxis. However, “mast cell histamine release inhibition” itself is not a discrete molecular target but rather encompasses multiple potential therapeutic strategies aimed at modulating immune responses mediated by these effector cells.

Other names

Inhibition of mast cell degranulationInhibition of mast cell mediator releaseMast cell stabilization

Mechanisms by which drugs inhibit mast cell histamine release include: - Stabilization of the mast cell membrane to prevent degranulation - Elevation of intracellular cyclic AMP levels in mast cells leading to reduced exocytosis of granules containing histamine - Inhibition of calcium influx required for exocytosis and mediator secretion from activated cells. - Interference with calmodulin activity necessary for cellular activation.