[Mechanisms of allergic asthma]

Abstract

The patho-physiology of allergic asthma is the result of several closely interrelated mechanisms. The hypersensitivity to mediation by IgE implies mast cell intervention and also by other non-mast cells possessing a receptor for Fc fragments of IgE. Their activation leads to the liberation of numerous mediators, some of which act directly on the bronchial smooth muscle fibres whilst others intervene by "pro-inflammatory effects". The other essential compound of asthma is non specific bronchial hyperreactivity. In reality the two phenomena are closely linked as is shown with changes in bronchial hyperreactivity after exposure or the inverse, by elimination of the allergen. The slow reaction linked to IgE by the cellular influx which it provokes in the airways amplifies the local inflammatory reaction and by this interacts with the autonomic nervous system.