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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 2 , ZnO, TiO 2 , and nanosilver of 20 nm (AgNP 20 ) or 70 nm (AgNP 70 ) diameters, only ZnO and AgNP 20 induced apoptosis. Caspases-7 and -9 were not activated by the tested NP while caspase-3 was activated by AgNP 20 only. However, both ZnO and AgNP 20 induced cytoskeletal breakdown as evidenced by the cleavage of lamin B 1 . Using an ELISArray approach for the simultaneous detection of several analytes (cytokines/chemokines), it was found that only ZnO and AgNP 20 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 20 induce apoptosis and cytokine production while others such as TiO 2 , CeO 2 , and AgNP 70 do not.

Palladium (Pd) is known to be released into the environment in the fine and ultrafine (at the nanoscale) airborne particle fractions mainly from automobile catalytic converters leading to an increase human exposure to this noble metal. It was reported that Pd can induce allergic reactions in individuals exposed to it via different ways. Some studies reported an increased number of eosinophils into airways following NP exposure in vivo in rodent models of allergies and inflammation. Knowing the importance of eosinophils in allergies, asthma and other lung diseases, it is surprising to observe that the direct effect of Pd at the nanoscale in eosinophils has been poorly documented. The aim of this study was to determine how Pd NPs will affect the biology of human eosinophils. Characterization of Pd NPs by dynamic light scattering indicates the presence of some aggregates when suspended in diverse solutions used here for the different experiments. Pd NPs did not significantly induce cell necrosis and apoptosis in eosinophils (0.5–150 μg/ml) as assessed by trypan blue exclusion assay, flow cytometry after staining with FITC-annexin V and propidium iodide and by morphological observations by optical microscopy. PD NPs, unlike the positive controls, did not induce reactive oxygen species (ROS) but were found to target the actin cytoskeleton, since actin was differently re-located intracellularly when compared to untreated cells as determined by fluorescence microscopy. Clearly, Pd NPs were found to increase adhesion of eosinophils onto human endothelial EA.hy926 cells. Using cytochalasin D, a cell-permeable and potent inhibitor of actin polymerization, this ability to increase adhesion was drastically reversed. Our results indicate that Pd NPs can target the cytoskeleton and increase the adhesion of human eosinophils by an actin-dependent mechanism. These findings show that human eosinophils can be activated by Pd NPs emphasizing the importance of fully investigating how these NPs could alter the biology of human cells involved in allergies, asthma and other lung diseases as well as in various other inflammatory disorders. [ABSTRACT FROM AUTHOR]