Early activation or "priming" of eosinophils in asthma.

Increased numbers of blood and tissue eosinophils are regularly observed in subjects suffering from bronchial asthma. The eosinophil number in the diseased organ is normally closely associated with the presence of clinical symptoms. Not only the cell number, but also the concentration of eosinophil-granule derived mediators is increased in the diseased organ. In particular toxic proteins released by the eosinophil may be responsible for the allergic inflammatory reaction and the concomitant tissue damage. Our recent investigations have shown that eosinophilic granulocytes from asthmatic individuals have the same phenotype as eosinophils from normal individuals (i.e. with respect to their density distribution pattern and surface receptor expression). In contrast, eosinophils from asthmatic individuals do possess increased metabolic activity (i.e. increased leukotriene C4 (LTC4) generating capacity and migration capacity). This increased metabolic activity is due to the presence of circulating factors, i.e. the cytokines interleukin 3 (IL-3), interleukin 5 (IL-5) and granulocyte-macrophage colony stimulating factor (GM-CSF). These cytokines are demonstrable in the circulation of asthmatic, but not normal individuals; they are synthetized by activated T-lymphocytes. This early activation, called "priming", should be the goal of future pharmacological endeavours in order to achieve more efficient treatment of asthma.