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Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance
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Researchers found that microplastics trigger a cascade of immune dysfunction in macrophages through toll-like receptor signaling, leading to disrupted glutathione metabolism and macrophage cell death via ferroptosis. In tumor-bearing mice, orally ingested microplastics accumulated in the lungs and remodeled the immune microenvironment over time, with increased infiltration of inflammatory macrophages and impaired lymphocyte function accompanying greater tumor burden.
Microplastics (MPs) are emerging contaminants whose immunological consequences remain poorly defined. Here, we investigated MP-induced immune responses using bone marrow-derived macrophages and a lung tumor model to delineate how MPs modulate tumor immunity. MPs triggered TLR2- and TLR4-dependent signaling pathways in macrophages, which initiated AP-1 signaling and lysosomal destabilization, followed by mitochondrial depolarization and excessive reactive oxygen species production. Despite NRF2 pathway activation, GPX1 and GPX3 were selectively suppressed, revealing a paradoxical uncoupling of glutathione metabolism that precipitated macrophage ferroptosis. In vivo, orally ingested MPs accumulated across multiple organs. In the lungs of tumor-bearing mice, MP exposure led to a time-dependent remodeling of the immune microenvironment, characterized by marked infiltration of M1-like macrophages and functional impairment of lymphocytes at later stages, which was accompanied by increased tumor burden. These findings identify an immune-redox-ferroptosis axis driven by glutathione imbalance and suggest redox disruption as a mechanistic link between microplastic exposure and tumor progression.
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Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
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Researchers investigated how microplastic exposure affects the immune response of macrophages to pneumococcal (Streptococcus pneumoniae) infection. They found that microplastics impaired macrophage phagocytosis, inhibited bacterial clearance, and amplified inflammation by activating ferroptosis and promoting M1 macrophage polarization through PI3K/Akt and MAPK/ERK signaling pathways. The study suggests that microplastic exposure may worsen bacterial lung infections by compromising immune cell function.
Inhaled Microplastics Inhibit Tissue Maintenance Functions of Pulmonary Macrophages
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Researchers found that inhaled microplastics accumulate in lung macrophages, the immune cells responsible for cleaning and maintaining lung tissue, and significantly impair their normal functions. The microplastic-laden macrophages showed reduced ability to perform tissue maintenance tasks that are essential for lung health. The study provides evidence that breathing in microplastics could compromise the lung's built-in defense and repair systems, with potential implications for respiratory health.
Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
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Mice that inhaled polystyrene microplastics for 60 days developed lung scarring, reduced lung function, and weakened lung barriers. The microplastics increased harmful bacteria in the lungs, which triggered an iron-related cell death process called ferroptosis -- revealing a new mechanism by which breathing in microplastics could cause lasting lung damage.
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.
Inhaled microplastics and lung health: Immunopathological effects and disease implications
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This review examines the molecular mechanisms by which inhaled microplastics damage lung health, focusing on oxidative stress, inflammation, and immune disruption. Researchers found that microplastics trigger reactive oxygen species production, deplete antioxidants, impair mitochondrial function, and compromise immune defenses in lung tissue. The evidence indicates that microplastics may also act as carriers for other toxic pollutants, amplifying respiratory health risks.
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