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Type II alveolar cells are highly robust in nature, yet susceptible to aerosolized nanoparticles (NPs). Dysfunction in these specialized cells, can often lead to emphysema, edema, and pulmonary inflammation. Long-time exposure can also lead to dangerous epigenetic modifications and cancer. Among the manufactured nanomaterials, metal oxide nanoparticles are widely encountered owing to their wide range of applications. Scores of published literatures affirm ZnO NPs are more toxic to human alveolar cells than TiO 2 . However, signalling cascades deducing differences in human alveolar responses to their exposure is not well documented. With A549 cells, we have demonstrated that epithelial to mesenchymal transition and an increased duration of phosphorylation of eIF2α are crucial mechanisms routing better tolerance to TiO 2  NP treatment over exposure to ZnO. The increased migratory capacity may help cells escape away from the zone of stress. Further, expression of chaperone such as Hsp70 is also enhanced during the same dose-time investigations. This is the first report of its kind. These novel findings could be successfully developed in the future to design relief strategies to alleviate metal oxide nanoparticle mediated stress.

Epithelial to Mesenchymal transition, eIF2α phosphorylation and Hsp70 expression enable greater tolerance in A549 cells to TiO2 over ZnO nanoparticles