Airway plasma exudation in detection of antiasthma drugs.

Increased numbers of cells and levels of cellular mediators in the airways may be without consequence or reflect tissue repair and can, therefore, not be equated with inflammation. Many tissue responses to inflammation are non-specific in that they are only exaggerations of base-line functions (blood flow, secretion, tone etc) which are stimulated also by non-inflammatory influences. In contrast, when there is plasma exudation in the airways this is a specific defence/inflammatory response. Accordingly, plasma exudation is not an increase in the normal capillary exchange of solutes but a dramatic increase in venular permeability. Plasma exudation is a graded response to mucosal inflammatory provocations and it is well correlated to symptoms in airway disease. The plasma exudate always crosses the epithelial lining to enter the airway lumen. Indeed, exudative indices in samples of airway surface liquids faithfully reflect intensity and time course of inflammatory processes in the underlying airway tissue. Drugs will reduce the exudation by any action that is a significant antiinflammatory effect, be it on recruitment/activation of cells on formation/release/action of mediators or directly on the permeability-regulating endothelial cells in the venular wall. The notion that plasma exudation is a significant pathogenetic mechanism in its own right in asthma does not reduce its instrumentality in the detection of new drugs to combat this disease.