In chemical terms the mediators of inflammation can be divided in amines (histamine, serotonine), peptides (ECF-A, bradykinin), proteins (lysosomal enzymes), and lipids. They mainly act at three levels: 1.) They induce vascular reactions and are responsible for the classical symptoms of inflammation, 2.) they define and modulate the cellular response towards the inflammatory stimulus such as the morphology of the tissue infiltrate, 3.) they act on haemostasis by interaction with platelets. While in the past investigations on classical mediators have dominated research, recently the biological role of lipid mediators has been appreciated. They can be detected only in minute quantities; they often have a short half-life and are not preformed within the cells. The most common precursor of the lipid mediators is arachidonic acid. This unsaturated fatty acid is generated from phospholipids after phospholipase activation of cells and is transformed by the enzyme cycloxygenase to a series of compounds such as the prostaglandins. They induce the classical signs of inflammation such asvescular dilatation, increase in permeability, pain, hyperalgesia etc. By the same process, the thromboxanes and prostacycline are generated which mainly act on the coagulation system. Various products are obtained from arachidonic acid via lipoxygenase activation. To these belong a factor chemically not completely defined with classical SRS-A activity; there is strong evidence that PAF and ECF are formed on the same line. Experiments in recent years have supported the idea that neutrophils and mononuclear cells are by far the main producers of lipid mediators, thus indicating the cellular interdependence during the inflammatory process.