Cell activation is accompanied by remodelling of its membrane components producing structurally diverse intracellular and extracellular lipids that seem to be essential in signal transduction, cell-cell communication, and as mediators in inflammation and pathophysiological mechanisms.1 Phospholipases are pivotal enzymes in the generation of these lipids, including eicosanoids (mostly prostaglandins), platelet activating factor (PAF), diacylglycerides, and other newly discovered bioactive autacoids.

PAF is a potent proinflammatory phospholipid mediator, involved in the pathogenesis of lung, liver, cardiovascular, renal, and other diseases.2 The gene coding for the human specific PAF receptor has recently been cloned from leucocytes showing homology to G protein coupled receptors.3

During the inflammatory arthritic process there are basically tissue damage phenomena combined with reparative processes. In brief, endothelial damage is followed by inflammatory cell infiltration in the perivascular area and synovial membrane. Furthermore, hyperplasia of synovial cells and accumulation of fibronectin and other matrix proteins are also seen. These morphological changes result from cellular interactions caused by a large variety of soluble mediators. We present information suggesting that PAF may be one of the important agents participating in these processes.