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Apical-Out Airway Organoids as a Pathophysiological Model To Study Macrophage-Mediated Epithelial Responses to Microplastics
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Development of Apical-out Airway Organoids to Evaluate Respiratory Toxicity of Polystyrene Microplastics
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Researchers developed apical-out airway organoids as an in vitro model to evaluate the respiratory toxicity of polystyrene microplastics, finding that microplastic exposure induced inflammation and barrier disruption in a model that better represents human airway exposure than standard cell cultures.
Apical-out airway organoids as a pathophysiological model to study macrophage-mediated epithelial responses to microplastics
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Scientists grew mini lung-airway tissue models in the lab to study how tiny plastic particles (microplastics) might affect our airways. They found that the plastics themselves didn't directly harm the airway tissue much, but when immune cells called macrophages "ate" small microplastic particles first, they released inflammatory signals that triggered mucus-producing cell changes in the airway tissue — suggesting the real damage from inhaled microplastics may come indirectly, through our immune system's response, rather than from the plastic particles touching our airways directly.
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Researchers used human airway organoids, an advanced lab model that mimics real lung tissue, to study the effects of microplastic fibers released from household clothes dryers. While the fibers did not stop organoid growth, they reduced the expression of a gene important for airway cell function and became physically embedded within the growing tissue. The study suggests that inhaled microplastic fibers could have long-term implications for lung tissue repair and establishes organoids as a valuable model for studying airborne plastic contamination.
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