Basophil platelet-activating factor release

Basophils Release Platelet-Activating Factor Instead of Histamine to Induce IgG-Mediated Systemic Anaphylaxis... 

Pinckard, R. N., Farr, R. S., and Hanahan, D. J. (1979) Physicochemical and functional identity of rabbit platelet-activating factor (PAF) release in vivo during IgE anaphylaxis with PAF Released in vitro from IgE sensitized basophils, J. Immunol. 123, 1847-1857. 

Allergic inflammation is characterized by an immediate immu-noglobulin-E-dependent mast cell and basophil degranulation leading to the release of mediators such as histamine that is responsible for most immediate manifestations of allergic disease. Other mediators include platelet-activating factor. 

The PMN cells include neutrophils, eosinophils, and basophils. Neutrophils make up 60-75% of circulating WBCs and provide the first line of defense against microbes that penetrate the normal barriers of skin. They are extremely efficient phagocytes and are a source of inflammatory cytokines and lipid mediators such as PGs, LTs, and platelet-activating factor. Eosinophils are involved in allergy and provide protection against parasites. Basophils contain vasoactive amines such as histamine, serotonin, and heparin, as well as precursors for PGs and LTs. Release of these pharmacological materials by the basophils is responsible for the anaphylactic reaction. These factors also serve as chemoattractants for neutrophils and eosinophils to sites of inflammation. 

Platelet-activating factor (PAE) is a glyceride-derived substance that is released by mast cells, alveolar macrophages, neutrophils, platelets, and other cells but not by basophils. It has potent bron-choconstrictor effects and also causes platelet aggregation and lysis. It attracts neutrophils and causes their activation. Also, PAE enhances vascular permeability and can cause pain, pruritus, and erythema. 

Epinephrine and isoproterenol (via cAMP mechanisms) and theophylline (via cAMP or block of adenosine receptors) inhibit the release of mediators from mast cells and basophils and cause bronchodilation. Diphenhydramine competitively blocks histamine actions at H, receptors, actions that would otherwise cause bronchoconstriction and increased capillary permeability. Dexamethasone has multiple cellular effects, including inhibition of IgE-producing clone proliferation, block of T helper cell function, and anti-inflammatory actions. Most of the actions of glucocorticoids result from decreases in the synthesis of cytokines (eg, interleukins, platelet activating factor) or eicosanoids (leukotrienes, prostaglandins). 

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