Prostaglandins surface activity

The principle underlying the BAT is that the attachment of the antigen to the IgE present on the surface of the basophil leads to the activation of the basophil and the release of its mediators (histamine, leukotrienes, prostaglandins, etc.) and the expression on its membrane of molecules such as CD63, CD203c or others which are markers of basophil activation. The basophils are identified with monoclonal antibodies marked with fluorochromes and anti-IgE and anti-CD63 receptors [for a complete review, we suggest readers read references 19-22]. 

Some effects of prostaglandins are mediated through cell surface G-protein coupled receptors (see Chapter ll).306 Some other prostanoids bind to and activate nuclear peroxisome proliferator-activated receptors.306 PGJ2 may inhibit fatty acid synthesis and fat deposition in adipose tissue through these receptors. Some of the prostanoid derivatives enter membranes and may become incorporated into phospholipids and exert their effects there. 

Arachidonic acid is not present in significant amounts in tissues as the free acid but is stored as a fatty acid at the sn-2 position of phospholipids. Prostaglandin biosynthesis is initiated by the interaction of a stimulus with the cell surface. Depending on the cell type, the stimulus can take the form of a hormone, such as angiotensin II or antidiuretic hormone, or a protease such as thrombin (involved in blood clotting), or both hormone and protease. These agents bind to a specific receptor that activates a phospholipase A2 that specifically releases the arachidonic acid from a phospholipid such as phosphatidylcholine. The release of arachidonic acid by phospholipase A2 is believed to be the rate-limiting step for the biosynthesis of eicosanoids. 

Blood-compatible polymer materials are required to inhibit both platelet adhesion and coagulation just as the endothelial on the polymer surface. It is known that there are many investigations in the design and the synthesis of socalled antithrombogenic materials. The immobilization of biologically active substances such as heparin [74, 75], urokinase [76], and prostaglandins [77-81] is one of the practical approaches. 

The difference between a normal immune response and a type I hypersensitive response is that in the latter, plasma cells secrete IgE. This class of antibody binds to Ec receptors on the surface of tissue mast cells and blood basophUs. Mast cells and basophUs coated by IgE are sensitised . Later exposure to the same allergen cross-links the bound IgE on sensitised cells, resulting in degranulation and the secretion of pharmacologically active mediators such as histamine, leukotrienes and prostaglandins. The principal effects of these products are vasodilation and smooth-muscle contraction (Table 15.6). 

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