Plasma Exudation in Asthma and Its Pharmacological Control

Abstract

Increased numbers of cells and elevated levels of cellular mediators in the airways may be without consequence or reflect tissue repair and can, therefore, not be equated with inflammation. Similarly, many tissue responses to inflammation (blood flow, secretion, smooth muscle tone, cough etc) are non-specific in that they are affected also by non-inflammatory influences. In contrast, when there is plasma exudation in the airways this is a specific defence/inflammatory response. Plasma exudation is not an increase in the normal capillary exchange of solutes but reflects 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 unfiltered plasma exudate crosses the epithelial lining to enter the airway lumen without disrupting the mucosa. Furthermore, the luminal entry occurs without compromising mucosal integrity as an absorption barrier. Exudative indices in samples of airway surface liquids faithfully reflect intensity and time course of inflammatory processes in the underlying airway tissue. Plasma exudation is a multipotential pathogenetic mechanism in asthma. Both through physical effects in tissue and lumen and through generation of potent plasma-derived peptide mediators the plasma exudate is a factor in the asthmatic diathesis. Drugs will reduce airway plasma exudation by any action that is a significant anti-inflammatory effect, be it on recruitment/activation of cells on formation/release/action of vasoactive mediators or directly on the permeability-regulating endothelial cells in the wall of postcapillary venules. Drug effects on the epithelial barrier to prevent mucosal exudation are not warranted.