Is childhood asthma an inflammatory disease?

There is now extensive evidence that asthma results from inflammation in large and small airways, and that the degree of inflammation reflects the clinical severity of the disease. Most of this evidence, however, has come from studies in adult patients. Evidence in children comes largely from indirect studies such as measurements of peripheral blood cells and inflammatory markers, rather than from direct bronchoscopic examination. Studies in adults show that inflammation in asthma is characterized by eosinophilia, epithelial damage, and bronchial hyperresponsiveness, and that activation of allergen-specific T cells plays an important role in orchestrating the inflammatory process. In children, indirect evidence of inflammation comes from the observation that anti-inflammatory agents such as inhaled corticosteroids improve symptoms and bronchial hyperresponsiveness, reduce the number of asthma exacerbations, and limit the progressive decline in lung function. Further evidence comes from measurements of nitric oxide and hydrogen peroxide (potential inflammatory markers) in exhaled air, and of inflammatory mediators in plasma and urine. As in adults, there is evidence that lymphocytes play an important role in orchestrating the inflammatory process. The immunologic profile appears to shift from a Th1-type cytokine profile to an allergen-related Th2-type profile prior to birth. Such a Th2 predominance constitutes a risk factor for the subsequent development of bronchial hyperresponsiveness and asthma in response to allergen.