Development of a nasal airway-on-chip co-culture model to study particulate matter exposure.

Abstract

Particulate matter (PM) is a major component of urban air pollution and is strongly associated with respiratory diseases. However, the mechanisms of PM-induced inflammation remain poorly understood due to a lack of physiologically-relevant airway models which can incorporate PM exposure. To address this, we used our nasal airway-on-chip platform to establish a co-culture model of human nasal epithelial cells and human pulmonary microvascular endothelial cells and used this model to investigate the effects of PM exposure on the nasal airway. In particular, we sought to understand the PM-induced reactive oxygen species (ROS)-mediated inflammatory response of the co-culture. Upon PM exposure, we observed a significant increase in ROS production consistent with oxidative stress-mediated injury. Additionally, treatment with the ROS scavenger <i>N</i>-acetyl-cysteine attenuated ROS levels and showed a trend toward reduced inflammation, suggesting a protective effect. These findings support the utility of our model for studying PM-induced airway inflammation in a more physiologically-relevant environment.