Figure 7.
Mechanism of activation and migration of blood eosinophils. NOX2 generates O2∙−, causing a depolarization and charge imbalance in eosinophils, which can be compensated by the antiporter activity of the CLC3. Superoxide may dismutate to hydrogen peroxide (H2O2) at low pH or in the presence of SOD. Being permeable, H2O2 can travel through the membrane and become H2O in presence of catalase or transform to a more oxidative hypochlorous acid (HOCl) through eosinophil peroxidase (EPO) in eosinophils. The activation of CLC3 leads to Cl− influx, resulting in shape change and cytoskeletal rearrangement in eosinophils and supporting the migration of eosinophils in response to cytokines/chemokines. Physical interaction of CLC3 to filamentous actin (F-actin) may also result in the cytoskeletal rearrangement and migration of eosinophils upon channel activation/phosphorylation.