[Mechanisms of bronchial hyperreactivity: role of airway inflammation and atopy]

The mechanisms of airway hyperresponsiveness are numerous and complex. The inflammatory process is one of the most important. It is characterized by epithelial damage and sloughing, by cellular infiltration of the bronchial mucosa and submucosa and by anatomical modifications of the bronchial wall. The cellular infiltrate is characterized by the presence of eosinophils, lymphocytes, monocytes-macrophages and mast cells. These cells are activated and release bronchoconstrictor and proinflammatory mediators. Eosinophils have toxic effects on the bronchial epithelium through the release of basic proteins, while lymphocytes play a central role through the release of cytokines, which can activate and recruit other cells. Mast cells have an important role of starter of the reaction but may also maintain it. Allergen inhalation in the laboratory, when a late response occurs, is responsible for an inflammatory reaction comprising eosinophil influx and activation and T lymphocyte activation. The intensity of the reaction is related to the transient increase in airway hyperresponsiveness confirming the important role of atopy and allergic reactions in airway hyperresponsiveness. However the same kind of inflammatory reaction can be present without atopy and antiinflammatory treatments, even if they reduce airway hyperresponsiveness, may not completely abolish it. This emphasises the complex mechanisms involved in persistent airway hyperresponsiveness.