Mediators of airway inflammation

Abstract

Mediators of inflammation can be classified into those that exist preformed in cells and those that are rapidly generated following stimulation. Vasoactive amines, lysosomal enzymes, neuropeptides and proteoglycans are examples of classes of mediators that are synthesized and stored, awaiting the proper stimulus that results in their release. Prostaglandins, leukotrienes, platelet activating factors and free radicals are representative substances that are generated as a result of cell activation. It is now clear that similar inflammatory mediators can be produced by diverse cell types. The exact role of specific mediators of inflammation depends on several factors: the precise stimulus that results in their release or production, the time in the overall inflammatory process when they are produced, and their specific biological effects. Upon stimulation, resident cells such as epithelial cells, mast cells and macrophages are in a position to induce inflammation, whereas cells entering sites of initial injury are able to perpetuate the process. Specificity further depends upon cell surface receptors and the mediators resulting from receptor perturbation. Finally, the most critical question is how inflammation, once induced, is limited by the mammalian system in order to prevent this process from unlimited extension. It would appear that numerous mechanisms which limit injury are brought into play with the induction of inflammation. These mechanisms include degradation of mediators by other mediators, mediator degradation by resident cells, and mediator dilution by tissue fluids. In summary, the role of mediators is extremely complex, involving their innate properties, temporal expression, and inactivation.