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Background  Inhaled nanoparticles can deposit in the deep lung where they interact with pulmonary cells. Despite numerous studies on pulmonary nanotoxicity, detailed molecular mechanisms of specific nanomaterial-induced lung injury have yet to be identified.    Results  Using whole-body dynamic inhalation model, we studied the interactions between aluminum oxide nanoparticles (Al 2 O 3  NPs) and the pulmonary system in vivo. We found that seven-day-exposure to Al 2 O 3  NPs resulted in emphysema and small airway remodeling in murine lungs, accompanied by enhanced inflammation and apoptosis. Al 2 O 3  NPs exposure led to suppression of PTPN6 and phosphorylation of STAT3, culminating in increased expression of the apoptotic marker PDCD4. Rescue of PTPN6 expression or application of a STAT3 inhibitor, effectively protected murine lungs from inflammation and apoptosis, as well as, in part, from the induction of chronic obstructive pulmonary disease (COPD)-like effects.    Conclusion  In summary, our studies show that inhibition of PTPN6 plays a critical role in Al 2 O 3  NPs-induced COPD-like lesions.    Electronic supplementary material  The online version of this article (10.1186/s12989-017-0234-0) contains supplementary material, which is available to authorized users.

Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway