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61,005 resultsShowing papers similar to Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
ClearInhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis imbalance
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.
Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance
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.
Mechanisms of exacerbation of Th2-mediated eosinophilic allergic asthma induced by plastic pollution derivatives (PPD): A molecular toxicological study involving lung cell ferroptosis and metabolomics
Researchers found that mice exposed to polystyrene microplastics combined with a common plastic additive (dibutyl phthalate) developed significantly worse allergic asthma symptoms, including increased airway inflammation driven by a specific type of immune response. The microplastics triggered a form of cell death called ferroptosis in lung cells, which amplified the allergic reaction. Treatment with an iron-binding drug provided relief, suggesting potential therapeutic approaches for people with asthma who are exposed to plastic pollution.
Microplastics exposed by respiratory tract and exacerbation of community-acquired pneumonia: The potential influences of respiratory microbiota and inflammatory factors
Researchers found that microplastics were present in the lungs of pneumonia patients, and that patients with severe pneumonia had higher levels of microplastics in their airways than those with milder cases. The microplastics appeared to worsen lung infections by disrupting the balance of airway bacteria and increasing inflammation. This study provides early evidence that inhaled microplastics may make respiratory infections more dangerous in humans.
Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling
Researchers found that mice exposed to polystyrene microplastics through their noses developed lung scarring (fibrosis) because the plastic particles triggered a form of cell death called ferroptosis, involving iron buildup and cell damage in lung tissue. Blocking the specific signaling pathway responsible (cGAS/STING) reduced the lung damage, pointing to a potential treatment approach if microplastic-related lung disease becomes a clinical concern.
Polystyrene Microplastics Induce Radiotherapy Resistance in Lung Cancer by Suppressing Ferroptosis Through NF-κB Activation
Researchers found that polystyrene microplastics impaired radiotherapy efficacy in lung cancer cells by suppressing ferroptosis—a form of iron-dependent cell death—through NF-κB activation, providing the first evidence that microplastics may contribute to cancer therapy resistance.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
Effects of micro- and nanoplastic exposure on macrophages: a review of molecular and cellular mechanisms
This review details how macrophages, key immune cells, respond when they engulf micro- and nanoplastics. The particles trigger inflammatory signaling, damage mitochondria and lysosomes, cause excessive production of harmful reactive oxygen species, and can lead to cell death, while in fat tissue they promote fat buildup and insulin resistance.
Mechanismof S‑Palmitoylationin Polystyrene Nanoplastics-Induced Macrophage Cuproptosis Contributingto Emphysema through Alveolar Epithelial Cell Pyroptosis
Researchers identified S-palmitoylation—a lipid modification process—as a key mechanism by which inhaled polystyrene nanoplastics trigger macrophage ferroptosis (iron-dependent cell death) in the lungs, providing a molecular explanation for how respiratory nanoplastic exposure damages immune cells.
Research Progress on Micro(nano)plastic-Induced Programmed Cell Death Associated with Disease Risks
This review summarizes how micro and nanoplastics can trigger different types of programmed cell death, including ferroptosis, pyroptosis, and apoptosis, based on recent animal and cell studies. These forms of cell death are linked to inflammation and diseases affecting the gut, liver, lungs, brain, and reproductive system. The findings help explain the biological mechanisms through which microplastic exposure could contribute to chronic disease in humans.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers investigated how macrophages, the immune cells that act as first-line defense in the gut and lungs, respond metabolically to polystyrene microplastic particles. The study found that phagocytosis of microplastics induced an immunometabolic active state in macrophages, suggesting that microplastic exposure may alter immune cell metabolism in ways relevant to understanding potential health effects.
Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen
Researchers found that polystyrene nanoplastics worsened the inflammatory damage caused by bacterial toxins in the spleens of mice. The nanoplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to cell death, and these effects were significantly amplified when nanoplastics were combined with bacterial endotoxin. The study suggests that nanoplastic exposure may compromise the immune system's ability to handle infections and inflammation.
Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp
Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.
Micro- and nanoplastics reduce the phagocytosis and intracellular killing of E. coli by THP1-Blue™ NFκB monocytes
Researchers exposed human immune cells to micro- and nanoplastic particles and then measured their ability to engulf and kill bacteria. They found that plastic exposure reduced both phagocytosis (the ability to capture bacteria) and intracellular killing in a dose-dependent manner, without directly killing the immune cells. The study suggests that microplastic exposure could weaken the body's first line of immune defense against bacterial infections.
Inhaled Microplastics Inhibit Tissue Maintenance Functions of Pulmonary Macrophages
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.
Polypropylene microplastic exposure leads to lung inflammation through p38-mediated NF- κB pathway due to mitochondrial damage
Researchers found that instilling polypropylene microplastic particles into mouse lungs caused dose-dependent increases in inflammatory cell counts, reactive oxygen species, and pro-inflammatory cytokines, with lung tissue analysis revealing the particles triggered inflammation via mitochondrial damage activating the p38-mediated NF-kB signaling pathway.
Detrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology
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.
Polystyrene nanoplastics lead to ferroptosis in the lungs
Researchers found that polystyrene nanoplastics trigger ferroptosis — a type of iron-driven cell death — in the cells lining the lungs by activating a stress signaling pathway (HIF-1α/HO-1), ultimately causing lung tissue injury. This adds to growing evidence that inhaled nanoplastics can directly damage respiratory tissue through oxidative cell death mechanisms.
Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury
Researchers found that inhaled polystyrene nanoplastics cause lung damage through a specific cell death process called ferroptosis, which involves iron buildup and oxidative stress in lung cells. The nanoplastics damaged mitochondria and triggered a chain reaction where the cell's iron storage was broken down, releasing harmful iron. Blocking this ferroptosis process with a drug called ferrostatin-1 reversed the lung damage in mice, pointing to a potential treatment approach.
Detrimental effects of micro- and nanoplastics (MNPs) on platelet and neutrophil immunity: Recent findings and emerging insights
Researchers reviewed how micro- and nanoplastics (MNPs) harm the immune system, finding that tiny plastic particles can trigger dangerous inflammation in platelets and neutrophils — immune cells that control clotting and infection defense. These effects could disrupt normal blood vessel function and immune balance, though the exact mechanisms by which cells take up MNPs remain poorly understood.
Small Plastics, Big Inflammatory Problems.
This review examined how micro- and nano-plastics trigger inflammatory responses through interactions with immune cells, finding that particles activate multiple signaling pathways including NF-kB and NLRP3 inflammasome, potentially contributing to chronic low-grade inflammation linked to cardiovascular disease, autoimmune disorders, and cancer.
Mitigating microplastic-induced organ Damage: Mechanistic insights from the microplastic-macrophage axes
This review is the first comprehensive examination of how microplastics interact with macrophages, the immune cells responsible for engulfing and removing foreign particles from the body. When macrophages absorb microplastics, the resulting oxidative stress disrupts their normal function, leading to inflammation and organ damage, with gut bacteria potentially playing a role in this harmful process.
Ferroptosis induced by environmental pollutants and its health implications
Researchers reviewed how environmental pollutants — including microplastics, PM2.5, and heavy metals — trigger ferroptosis, a form of programmed cell death driven by iron and fat oxidation, finding that targeting this cell death pathway could be a strategy to reduce organ damage caused by pollution exposure.