Based on a growing body of evidence, allergic as well as intrinsic
bronchial asthma have recently been defined as chronic persistent inflammatory disorders. Agreement has been reached that
asthma can no longer be equated with
bronchospasm only, and that the absence of reversibility of airflow obstruction does not exclude
bronchial asthma.
Bronchial hyperreactivity, on the other hand, although common to the vast majority of asthmatics, is not specific for
bronchial asthma and provocation tests to measure
bronchial hyperreactivity are not suited for routine monitoring of
bronchial asthma. The clinical features of
asthma are related to cellular as well as to soluble parameters of bronchial
inflammation. Therefore, means of assessing and monitoring asthmatic
inflammation have been investigated. Since eosinophils, T lymphocytes, mast cells, macrophages, neutrophils, epithelial cells, and structural cells, as well as various proinflammatory mediators and
proteins, have been implicated in the pathogenesis of
bronchial asthma, it has been anticipated that several of these cells or mediators might be either diagnostic of
bronchial asthma or could serve as markers to monitor the underlying bronchial
inflammation. Currently there is no diagnostic marker of
bronchial asthma, which, on its own, either confirms or excludes
bronchial asthma with appropriate sensitivity and specificity. Clinically the most reliable feature of
bronchial asthma that seems to be related closely to the symptomatology still is the presence of eosinophils in peripheral blood, and especially in sputum. Eosinophil-derived products, particularly
eosinophil granule proteins, have been investigated as markers of eosinophil participation in the pathogenesis of
asthma and, comparable to eosinophil numbers themselves, are possible predictors of impending exacerbations of allergic, as well as intrinsic
bronchial asthma. However, clinically their precise value in diagnosing and monitoring of
bronchial asthma has not been documented convincingly and requires further investigation. Increasing data suggest that the regulation of
eosinophilia is largely conveyed by
interleukin-5 (IL-5) released from activated T-helper lymphocytes and possibly other cells. Therefore, T-lymphocyte activation, and especially assessment of systemic and local
IL-5 levels, might be of diagnostic value and possibly useful in monitoring of
inflammation in
bronchial asthma in the future. A possible role and future applications for other markers of
inflammation not related to eosinophils in monitoring or diagnosing
bronchial asthma need to be established.