Mediatorfrigivelse

Mediatorfrigivelse is the release of chemical mediators by cells in response to stimuli, a central process in inflammation and immune responses. Mediation can involve preformed mediators stored in granules as well as newly synthesized substances produced after activation. In many tissues, mast cells and basophils store mediators such as histamine, proteases, and other compounds that can be released rapidly through degranulation. Other cells, including eosinophils, platelets, macrophages, and endothelial cells, contribute to mediator release through various secretory pathways.

Mechanisms underlying mediatorfrigivelse include exocytosis of granules, vesicular transport, and de novo synthesis of mediators. Triggers encompass allergen exposure with IgE cross-linking, complement activation (for example C3a and C5a), physical injury, cytokines, and pathogen-associated signals detected by innate receptors. The specific mediators released and the timing of their release depend on the cell type and stimulus.

Common mediators and their effects include histamine and proteases, which promote vasodilation and increased vascular permeability; prostaglandins and leukotrienes, which can cause bronchoconstriction, pain, and fever; cytokines and chemokines, which coordinate immune cell recruitment and activation. The net result is local inflammation, recruitment of leukocytes, and, in some contexts, systemic responses such as anaphylaxis.

Clinical relevance and regulation focus on conditions where mediatorfrigivelse contributes to symptoms, such as allergic reactions and asthma. Therapies often aim to limit mediator release or block mediator receptors, including antihistamines, corticosteroids, leukotriene antagonists, and, in acute reactions, rapid interventions like epinephrine. In research, mediatorfrigivelse is studied to understand inflammatory processes and to test potential treatments.