In patients with asthma, inhibition of neural output from receptors in the airways has been shown to prevent interleukin (IL)-5 mediated eosinophil activation by cytokines, minimize IL-3, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF) mediated eosinophil survival, and diminish subsequent inflammation of the airways caused by damage to epithelial and smooth muscle cells (10). Here, IL5 is linked to asthma.