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.