[The concept of mediators in acute inflammatory reactions]

The evolution of ideas about inflammation oscillates between two poles: sometimes the cell aspects of inflammation are described, with leucocyte adhesion to the vessel wall followed by migration into the tissues and phagocytosis - at other times it is the turn of the chemical intermediaries accounting for the damage to blood vessels, in which case vasodilatation, permeability and chemotaxis are given particular emphasis. The present tendency is to concentrate on the origin of these intermediaries and their relationship to the different cell populations found in situ. Before defining the relationship between cells and acute inflammatory mediators, an inventory needs to be drawn up of the latter. They can be divided into three main categories, according to the manner of their involvement at the site of inflammation: preformed agents, which are then released; mediators formed as a result of enzyme influences, cell-derived or not, from inactive precursors; the enzymes themselves which attack the structures involved in the lesion. These various mediators are thus traceable to specific mechanisms of formation or release, from cell populations that are now clearly identified. From an understanding of how the inflammatory focus has been colonised by the different leucocyte populations and a knowledge of their enzymatic potential, conclusions can be drawn not only about the mediators concerned but more especially about the pharmacological agents that must be mobilised in order to neutralise their clinically apparent effects.