Abstract

Among the 'allergic' conditions involving the lung, asthma is the more frequent and the most extensively investigated, although asthma itself may be caused by different disorders. The triggering event in allergic subjects is the reaction allergen-specific immunoglobulin E (IgE) that activates mast cells and initiates a complex and redundant inflammatory process, where cells, cytokines and adhesion molecules are involved at different stages. In fact, mucosal eosinophilic inflammation is one of the distinctive features of asthma and the particular T helper type 2 (Th2) phenotype of allergic patients favours it. In general, the clinical severity of asthma correlates well with the degree of inflammation. None the less, other phenomena such as non-specific bronchial hyperresponsiveness and remodelling intervene in the pathophysiology of allergic asthma. These phenomena are only partially inflammation-related. In particular, the remodelling of the bronchial wall seems to start very early in life and also seems to be a distinctive histological feature of the asthmatic bronchus. The recent introduction of biological treatments (monoclonal antibodies) has allowed elucidation of some of the pathogenic features of allergic asthma.

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