Nitric oxide-induced eosinophil apoptosis is dependent on mitochondrial permeability transition (mPT) JNK and oxidative stress: apoptosis is preceded but not mediated by early mPT-dependent JNK activation

摘要

BackgroundEosinophils are critically involved in the pathogenesis of asthma. Nitric oxide (NO) is produced in high amounts in asthmatic lungs and has an important role as a regulator of lung inflammation. NO was previously shown to induce eosinophil apoptosis mediated via c-jun N-terminal kinase (JNK) and caspases. Our aim was to clarify the cascade of events leading to NO-induced apoptosis in granulocyte macrophage-colony stimulating factor (GM-CSF)-treated human eosinophils concentrating on the role of mitochondria, reactive oxygen species (ROS) and JNK.