Inflammation platelet-activating factor

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

These cells respond to a number of different chemoattractants which have specific and distinct receptors on the membrane surface (for recent reviews see Refs. 3 and 4). Such chemoattractants include N-formylpeptides, which are bacterial peptides, and mediators of inflammation such as leukotriene B4, C5a, and platelet activating factor. 

Platelet-activating factor A mediator of platelet aggregation and inflammation that is produced in response to stimuli, such as white blood cells. 

It is possible that nematode-secreted AChEs act on alternative substrates to ACh. We had previously suggested, on the basis of structural similarity, that platelet-activating factor (PAF), a potent phospholipid mediator of inflammation, might represent such an alternative substrate (Blackburn and Selkirk, 1992b) but subsequent studies demonstrated that purified AChEs did not cleave PAF, and the enzyme responsible for this activity in secreted products of N. brasiliensis, PAF acetylhydrolase, was purified and defined as a distinct heterodimeric protein (Grigg et al., 1996). Although an open mind on the subject sould be kept, the strict substrate specificity of the nematode-secreted AChEs suggests that they most likely act on ACh alone. 

Eicosanoids, Docosanoids, Platelet-Activating Factor and Inflammation... 

It is a cromolyn analogue. It is an antihistaminic (H antagonist) and probably inhibits airway inflammation induced by platelet activating factor (PAF) in primate. It is not a bronchodilator. It is used in asthma and symptomatic relief in atopic dermatitis, rhinitis, conjunctivitis and urticaria. It is absorbed orally and well tolerated. Bioavailability is 50% due to first pass metabolism and is primarily metabolized. The common side effects include dry mouth, sedation, dizziness and nausea. 

Develop normally and are healthy. No difference in their reaction to endotoxin shock, however resist the lethal effects of shock induced by platelet-activating factor. Inflammation induced by arachidonic acid is markedly reduced (Chen et al. 1994 Argentieri et al. 1994). 

Platelet-activating factor or l-alkyl-2-acetyl- n-glycero-3-phosphocholine is an ether analog of phosphatidylcholine. This biologically active lipid is of great current interest. Initially, it was found to affect aggregation of platelets and to induce a hypertensive response at very low concentrations. Recent research has revealed its role as a mediator of inflammation and of other physiologic effects on many different types of cells. 

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. 

Zimmerman, G.A., Prescott, S.M. and McIntyre, T.M. (1992). Platelet activating factor. A fluid phase and cell associated mediator of inflammation. In Inflammation Basic Principles and Clinical Correlates (eds J.I. Gallin, I.M. Goldstein and K Snyderman), pp. 149-176. Raven Press, New York. 

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