Abstract
Fine dust particles in the air travel into our body via the airway tract and cause severe respiratory diseases. Thus, the analysis of the effects of dust particles on the respiratory system has been receiving significant research interest. However, most studies on the toxicity of dust particles involve two-dimensional (2D) cell cultures, animal models, and epidemiology. Here, we inkjet-printed athree-dimensional (3D) alveolar barrier model to study how dust particles cause respiratory diseases. The three-layered in vitro model was exposed to A2 fine test dust with varying concentrations and exposure durations. The results highlighted the destruction of the tissue architecture along with apoptosis in the bioprinted alveolar barrier. The damage at the cellular level induced an increase in the amount of pro-inflammatory cytokines secreted, followed by triggering of the signal transduction pathway and activation of transcription factors. As a consequence of the release of cytokines, the extracellular matrix was degraded, which led to the collapse of the cell structure, loss of cell polarity, and a decrease in barrier tightness. Further, the pulmonary surfactant protein-related genes in the dust-treated alveolar tissue were investigated to evaluate the possible role of dust particles in pulmonary surfactant dysfunction. This study demonstrated the use of 3D-printed tissue model to evaluate the physiological impact of fine dust particles on cytotoxicity, alveolar barrier rigidity, and surfactant secretion of an alveolar barrier.
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