CELLULAR AND IMMUNOLOGICAL MARKERS OF ALLERGIC AND INTRINSIC BRONCHIAL-ASTHMA

Based on a growing body of evidence, allergic as well as intrinsic bro nchial asthma have recently been defined as chronic persistent inflamm atory disorders. Agreement has been reached that asthma can no longer be equated with bronchospasm only, and that the absence of reversibili ty of airflow obstruction does not exclude bronchial asthma. Bronchial hyperreactivity, on the other hand, although common to the vast major ity of asthmatics, is not specific for bronchial asthma and provocatio n tests to measure bronchial hyperreactivity are not suited for routin e monitoring of bronchial asthma. The clinical features of asthma are related to cellular as well as to soluble parameters of bronchial infl ammation. Therefore, means of assessing and monitoring asthmatic infla mmation have been investigated. Since eosinophils, T lymphocytes, mast cells, macrophages, neutrophils, epithelial cells, and structural cel ls, as well as various proinflammatory mediators and proteins, have be en implicated in the pathogenesis of bronchial asthma, it has been ant icipated that several of these cells or mediators might be either diag nostic of bronchial asthma or could serve as markers to monitor the un derlying bronchial inflammation. Currently there is no diagnostic mark er of bronchial asthma, which, on its own, either confirms or excludes bronchial asthma with appropriate sensitivity and specificity. Clinic ally the most reliable feature of bronchial asthma that seems to be re lated closely to the symptomatology still is the presence of eosinophi ls in peripheral blood, and especially in sputum. Eosinophil-derived p roducts, particularly eosinophil granule proteins, have been investiga ted as markers of eosinophil participation in the pathogenesis of asth ma and, comparable to eosinophil numbers themselves, are possible pred ictors of impending exacerbations of allergic, as well as intrinsic br onchial asthma. However, clinically their precise value in diagnosing and monitoring of bronchial asthma has not been documented convincingl y 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 cell s. Therefore, T-lymphocyte activation, and especially assessment of sy stemic and local IL-5 levels, might be of diagnostic value and possibl y useful in monitoring of inflammation in bronchial asthma in the futu re. A possible role and future applications for other markers of infla mmation not related to eosinophils in monitoring or diagnosing branchi al asthma need to be established.