ABSTRACT
AIRWAY INFLAMMATION IN CHRONIC STABLE ASTHMA
Together with mast cells and eosinophils, airway infiltration with T-helper type 2 (Th2) CD4+ T lymphocytes is a central feature of asthma pathophysiology. Although T lymphocytes are less numerous in sputum than in bronchial biopsies or bronchoalveolar lavage (BAL), and usually represent less than 3% of sputum cells, these cells have been successfully phenotyped using flow cytometry. Asthmatics have a slightly raised number of CD4+ T cells expressing surface activation markers such as intercellular adhesion molecule-1 (ICAM-1) (Figure 4.2). Studies have also shown a reduced proportion of lymphocytes expressing the marker CD16 identifying these as natural killer (NK) cells. Raised B lymphocyte counts have been shown to correlate with sputum eosinophil counts (Figure 4.3). In keeping with this, increased amounts of secretory immunoglobulin A (IgA) have been detected in the sputum of asthmatics, which forms complexes with
interleukin (IL)-8. These correlate with the number of sputum eosinophils and their extent of activation (Figure 4.4). Further interest in IgA in asthma has arisen from a study showing that asthmatics had higher levels of sputum IgA that were not only directed towards mite allergen but also towards Streptococcus pneumoniae antigen (Figure 4.5). Interestingly, the IgA levels correlated with the extent of local eosinophil activation, as reflected in sputum ECP levels; lending support to the hypothesis that secretory IgA may act as a potent activator for airway eosinophils.
