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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.
systems that separate direct epithelial particle contact from immune-cell-mediated paracrine effects remain limited. Here, we generated human airway basal stem cells (hABSCs)-derived apical-out airway organoids (AOAOs) with outward-facing ciliated surfaces and used them to evaluate operationally size-fractionated, polydisperse polystyrene microplastic (PS-MP) fractions. PS-MPs were characterized by laser diffraction, SEM, FT-IR, Nile red labeling, endotoxin testing, and culture-media stability/protein-adsorption assays. AOAOs were exposed under two submerged configurations: direct application of PS-MPs to the organoid surface or indirect exposure to conditioned media from PS-MP-treated THP-1-derived macrophages. CCK-8, MTT, and LDH range-finding assays identified 1 and 100 μg/mL as non-cytotoxic nominal submerged doses for macrophage-organoid experiments. Direct exposure of AOAOs to small, medium, or large PS-MP fractions did not induce marked TNF-α expression, mucin secretion, epithelial barrier disruption, or goblet cell hyperplasia. In contrast, the small PS-MP fraction showed the strongest macrophage association and induced extracellular IL-1β release; conditioned media from small PS-MP-exposed macrophages increased TNF-α expression and Muc5ac-positive goblet cell populations in AOAOs. Selective caspase-1 activation in the small 100 μg/mL condition, together with cleaved GSDMD immunoreactivity and LDC7559-sensitive IL-1β release, supported a caspase-1-associated, GSDMD-sensitive component of IL-1β secretion, but did not establish definitive canonical inflammasome activation. This AOAO platform provides a submerged mechanistic proof-of-concept for dissecting macrophage-conditioned airway epithelial remodeling by PS-MPs, while not representing aerosol deposition or inhalation-equivalent dosimetry.
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Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
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.
Pathophysiological effects of inhaled airborne microplastics on the respiratory epithelial barrier: A review
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Tiny plastic particles floating in the air we breathe may be doing more damage to our lungs than we realized. This review of existing research found that when these microplastics land in our airways, they can trigger cell stress, inflammation, and damage to the protective lining of our lungs—potentially making respiratory problems worse over time. While scientists still need more long-term studies to fully understand the risks, this research is an early warning sign that the plastic pollution in our air isn't just an environmental issue—it could be a health issue too.
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