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PersonalizedPathogenic Nanoplastic Coronas OrchestrateEfferocytosis-Driven Immune Evasion in Lung Adenocarcinoma
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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.
More Papers Like This
Personalized Pathogenic Nanoplastic Coronas Orchestrate Efferocytosis-Driven Immune Evasion in Lung Adenocarcinoma
AI summary Read the abstract
When tiny plastic particles from PET (a common plastic in bottles and clothing) get inhaled, they pick up proteins from lung fluid that essentially disguise them—and in mice with lung cancer, this disguise helped tumors grow faster by tricking the immune system into "cleaning up" cancer cells in a way that actually protects the tumor instead of fighting it. This matters because it suggests breathing in airborne microplastics could make existing lung cancer worse by hijacking the body's normal immune defenses, giving scientists a new potential target for treatment and another reason to take plastic pollution seriously as a health risk
A93-04 Microplastics Induce Bioenergetic Dysfunction and Impair Macrophage-mediated Anti-tumor Immunity
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Tiny plastic particles that we breathe in every day may weaken the immune cells in our lungs that normally hunt down and destroy cancer cells, according to a new mouse and lab-based study. Researchers found that these microplastics get stuck inside lung immune cells (macrophages), disrupt their energy production, and trigger changes that make them worse at fighting tumors—and mice exposed to microplastics developed larger tumors afterward. While this research is still early and hasn't been proven in humans, it offers a possible clue as to why lung cancer is rising in people who have never smoked.
Nuclear accumulation of stabilized SPDEF drives nanoplastic-induced lung adenocarcinoma progression through sustaining inflammation via TRIB3–c-Fos signaling
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Scientists exposed lung cancer cells and mice to nanoplastics (tiny plastic particles from broken-down plastic pollution) at levels similar to what people might realistically encounter, and found that long-term exposure sped up lung tumor growth. They traced this to a chain reaction inside cells—a protein called SPDEF builds up and triggers ongoing inflammation—that appears to fuel cancer progression. While this research was done in cells and mice rather than humans, it adds to growing evidence that everyday plastic pollution exposure may carry real cancer-related risks worth taking seriously.
Microplastic-induced carcinogenesis: Molecular mechanisms, cellular interactions, and toxicological implications
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Tiny plastic particles that we breathe, eat, and touch every day are now showing up in our blood, lungs, and other organs, and this review of existing research explains how they might contribute to cancer. Microplastics can trigger cell damage, inflammation, and disrupted signaling in ways linked to tumor growth, and they can also act like tiny rafts that ferry other harmful chemicals and toxins deeper into our bodies. While scientists haven't proven microplastics directly cause cancer in humans yet, the mounting evidence is a strong signal that reducing plastic exposure and pushing for more research should be a public health pri
Contribution of Cancer-Specific Protein Coronas to the Pro-Tumor Effects of Nanoplastics through Enhanced Cellular Interactions
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Researchers investigated how nanoplastics interact with blood proteins to form a protein coating that changes how the particles behave around cancer cells. They found that this protein coating enhanced the uptake of nanoplastics by cancer cells and could promote tumor-related behaviors. The study raises important questions about whether nanoplastic exposure could influence cancer progression through these protein-mediated interactions.
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