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Environmentally Relevant Microplastic Inhalation Drives Pulmonary Fibrosis via a FABP5–FOXK2–PDGFA Macrophage Axis

ABSTRACT: Microplastics are increasingly detected in the atmosphere and human tissues, yet their long-term effects on lung biology remain unclear. Here, we identified multiple microplastic polymers in human lung tissues using pyrolysis–gas chromatography/mass spectrometry (Py-GC/MS). Using a chronic inhalation model with environmentally relevant concentrations, we show that microplastic exposure induces progressive pulmonary fibrosis in a particle size–dependent manner, with nanoscale particles producing stronger fibrogenic effects than micron-scale particles. Single-cell transcriptomics revealed expansion of Fabp5⁺ interstitial macrophages and early fibroblast activation specifically following nanoscale exposure. Cell–cell communication analysis identified PDGFA–PDGFRA signaling as a key mediator of macrophage–fibroblast interactions. Mechanistically, nanoscale microplastics activated a Fabp5–FOXK2–PDGFA transcriptional axis in macrophages, whereas micron-scale particles showed minimal activation. Fabp5 silencing suppressed this pathway and attenuated pulmonary fibrosis, revealing a macrophage-driven mechanism linking inhaled microplastics to fibrotic lung remodeling.

ORGANISM(S): Mus musculus

PROVIDER: GSE324602 | GEO | 2026/03/16

REPOSITORIES: GEO

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Project description:The pollution of the environment with microplastics has been recognized as an emerging threat worldwide. Due to an exponential increase in production of plastic over the last eight decades and its longevity in the environment, accumulating amounts of microplastic are polluting rivers, lakes and the ocean. Their entry pathways are diverse and still only incompletely understood. Since microplastics are usually defined smaller than 5 mm, it can be ingested by a wide range of aquatic organisms including teleost fish. There are different approaches to study the detrimental effects of pollutants on aquatic organisms. On the one hand, generic baseline parameters such as growth and mortality are regularly considered, often accompanied by established stress parameters such as cortisol, heat shock proteins or lipid oxidation. The conflicting findings to date suggest that these parameters might not be sensitive enough to indicate the physiological effects of environmentally relevant microplastic concentrations. For this reason, more sophisticated biological approaches could provide new insights into whether and how microplastics harm fish. To date, proteomic approaches have been used only sporadically when investigating the effects of microplastic exposure on aquatic organisms. So far, this approach has not been used to address potential microplastic impacts in fish. In the present study, a proteomic approach was trialed alongside established methods in an investigation of fish experiencing long-term exposure to environmentally relevant concentrations of microplastics. Two groups of rainbow trout (Oncorhynchus mykiss were exposed to microplastic concentrations and sizes currently encountered in wild fish and an increased concentration, expected to occur in the near future. These groups where compared to a control group maintained in MP free conditions. Five fish of each treatment were sampled at three time points (week 1, week 4, week 17). The experiments were performed in triplicates, resulting in 45 samples used in the proteomic analysis.

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Environmentally Relevant Microplastic Inhalation Drives Pulmonary Fibrosis via a FABP5–FOXK2–PDGFA Macrophage Axis

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