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PersonalizedPathogenic Nanoplastic Coronas OrchestrateEfferocytosis-Driven Immune Evasion in Lung Adenocarcinoma
Summary
Scientists found that when tiny plastic particles (from common plastic bottles) are inhaled, they pick up a coating of proteins from the lungs that essentially "reprograms" the immune system to help lung cancer grow faster and hide from immune attack. In mice, this plastic-protein combo boosted tumor growth by helping cancer cells get eaten and cleared in a way that shuts down the body's cancer-fighting T-cells—and blocking a key protein in this process reversed the effect. While this research was done in mice and lab samples rather than in living patients, it adds to growing evidence that breathing in microplastics isn
Airborne nanoplastic (NP) pollution is an emerging threat to respiratory health. Although inhaled NPs rapidly acquire a protein corona that shapes their bioactivity, the consequences of this process in cancer-susceptible lungs remain unclear. Here, we investigated whether NPs form a disease-specific pathogenic protein corona in lung adenocarcinoma that rewires immune signaling and accelerates tumor progression. Polyethylene terephthalate (PET) NPs were generated by mechanical fragmentation and extensively characterized. In tumor-bearing mice, inhaled PET NPs accelerated tumor growth relative to controls. Proteomic analysis of PET NPs incubated with bronchoalveolar lavage fluid from patients with lung adenocarcinoma identified lysozyme (LYZ) as a selectively enriched corona component associated with tumor stage and metastasis. Corona formation induced conformational remodeling of LYZ, enhanced its enzymatic activity, and prolonged its membrane retention. Mechanistically, corona-bound LYZ engaged Toll-like receptor 4 and activated a PGRN–LXRα signaling axis, thereby increasing lysosomal acidification–dependent efferocytosis, promoting M2 macrophage polarization, and reducing CD8+ T-cell infiltration. In vivo, AAV9-mediated knockdown of LYZ or PGRN attenuated PET NP-induced efferocytosis, reversed immunosuppressive reprogramming, restored CD8+ T-cell infiltration, and suppressed tumor growth, demonstrating the functional requirement for this corona pathway. These findings establish disease-derived PET NP coronas as active nano–bio interfaces that connect environmental PET NP exposure with efferocytosis-driven immune evasion in lung adenocarcinoma. This work provides a mechanistic link between airborne NPs and tumor progression in susceptible hosts and highlights corona-mediated signaling as a potential therapeutic target and environmental health concern.