Cytokine-stimulated human lung alveolar epithelial cells release eotaxin-2 (CCL24) and eotaxin-3 (CCL26).

Asthma is a complex inflammatory disease characterized by a prolonged underlying airway inflammation resulting from cytokine-orchestrated signaling between many types of cells, including airway epithelial cells. Trafficking, recruitment, and activation of cells in airway disease are, in part, modulated by the newly discovered CC subfamily of chemokines, eotaxin (CCL11), eotaxin-2 (CCL24) and eotaxin-3 (CCL26), which transduce signals by acting as agonists for the CCR3 receptor. The specific cytokine stimuli that modulate CCL24 and CCL26 release in airway epithelial cells remain poorly defined.