Airway inflammation, bronchial reactivity and asthma.
Asthma is a common disease of children the basis of which is a state of chronic immunological inflammation which causes bronchial hyperreactivity and renders the patient liable to develop widespread airways obstruction in response to a variety of stimuli. In many instances it is likely that the immunological inflammation results from ongoing antigenic stimuli with the release of chemical mediators responsible for short term bronchospasm and cytokines responsible for the ongoing inflammatory process. Other insults can apparently result in very similar immunological events in asthmatics, particularly viral infections and a similar process can be initiated in children without asthma, including those with chronic bacterial infections of the lungs. There are differences in the bronchial hyperreactivity of asthma and other diseases which suggest that in the asthmatic the mast cell is either different structurally or functionally and this renders the patient susceptible to exercise induced asthma in addition to the bronchial hyperreactivity to chemical mediators common to a number of diseases with hyperreactivity. There is good evidence of direct genetic control of atopy and the large majority of children with asthma are atopic but there is no direct genetic link between atopy and asthma and twin studies strongly suggest the existence of a 'permissive' asthma gene which will allow the disease to develop if there is an appropriate external trigger. The only drugs which have been shown to significantly reduce bronchial reactivity are the corticosteroids with a lesser effect noted for sodium cromoglycate and nedocromil. Inhaled corticosteroids can reverse the immunologic inflammatory process and reduce bronchial reactivity, sometimes to normal levels, but on stopping treatment the patient reverts back to the asthmatic state. At the present time it appears that controlled longterm inhaled corticosteroid therapy is the most rational treatment for significant perennial childhood asthma.
Godfrey
S
S
Institute of Pulmonology, Hadassha University Hospital, Jerusalem.
D000402:Airway Obstruction / Q000209:etiology*; D001249:Asthma / Q000150:complications* / Q000235:genetics / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000188:drug therapy / Q000209:etiology*; D002648:Child; D006801:Humans; D007249:Inflammation / Q000276:immunology; D008957:Models, Genetic