Activation of human AML14.3D10 eosinophils by nanoparticles: Modulatory activity on apoptosis and cytokine production.

Eosinophilic inflammation is frequently observed in response to nanoparticle (NP) exposure in airway rodent models of allergies where the number of eosinophils is increased in lungs. Despite this, it is surprising that the potential cytotoxic effect of NP, as well as their direct role on eosinophils is poorly documented. The present study investigated how different NP can alter the biology of the human eosinophilic cell line AML14.3D10. It was found that among NP forms of CeO, ZnO, TiO, and nanosilver of 20 nm (AgNP) or 70 nm (AgNP) diameters, only ZnO and AgNP induced apoptosis. Caspases-7 and -9 were not activated by the tested NP while caspase-3 was activated by AgNP only. However, both ZnO and AgNP induced cytoskeletal breakdown as evidenced by the cleavage of lamin B. Using an ELISArray approach for the simultaneous detection of several analytes (cytokines/chemokines), it was found that only ZnO and AgNP increased the production of different analytes including the potent pro-inflammatory CXCL8 (IL-8) chemokine. From the data here, we conclude that toxic effects of some NP could be observed in human eosinophil-like cells and that this could be related, at least partially, by induction of apoptosis and production of cytokines and chemokines involved in inflammation. The results of this study also indicate that distinct NP do not activate similarly human eosinophils, since ZnO and AgNP induce apoptosis and cytokine production while others such as TiO, CeO, and AgNP do not.