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61,005 resultsShowing papers similar to Polystyrene Microplastics Induce Inflammatory Responses and Promote M2‐Associated Cytokine Expression in Mouse Lung Tissues
ClearExposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Oropharyngeal Administration of Polystyrene Microplastics Induces Profibrotic and Oxidative Changes in Murine Lung Tissue
Researchers investigated the early lung effects of inhaled polystyrene microplastics in mice over a 21-day exposure period. While overall fibrosis scores did not reach statistical significance in this short timeframe, they observed significant macrophage infiltration, active particle uptake by immune cells, and upregulation of oxidative stress and fibrosis-related molecular markers. The findings suggest that microplastic inhalation triggers early immune and oxidative responses that may precede lung tissue remodeling.
Polystyrene particles induces asthma-like Th2-mediated lung injury through IL-33 secretion
Researchers found that inhaled polystyrene microplastic particles triggered asthma-like inflammation in the lungs of mice, with smaller particles causing more severe responses. The particles stimulated the release of IL-33, a signaling molecule that activates a specific type of immune response associated with allergic airway disease. The study identifies a potential mechanism by which airborne microplastics could contribute to respiratory inflammation.
Sterile inflammation induced by respirable micro and nano polystyrene particles in the pathogenesis of pulmonary diseases
Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
Size-Dependent PulmonaryToxicity and Whole-Body Distributionof Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
Researchers used a whole-body inhalation exposure system to chronically expose male mice to polystyrene micro- and nanoplastics at environmental concentrations and tracked particle distribution and lung toxicity. Nanoplastics (80 nm) showed greater tissue transport than microplastics (1 µm), with highest accumulation in lungs followed by blood and spleen, and both sizes disrupted oxidative balance and antioxidant defenses.
Pulmonary accumulation and immune modulation by intravenously administered environmentally relevant microplastics in mice
Researchers intravenously administered environmentally relevant oxidized polyethylene microplastics to mice and tracked their distribution using fluorescent labeling. The particles primarily accumulated in the lungs and induced inflammatory cell infiltration, demonstrating that microplastics entering the bloodstream can concentrate in pulmonary tissue and trigger immune responses.
Size-dependent toxicity of polystyrene microplastics in lung cells: An in vivo and in vitro study
Researchers investigated the size-dependent toxicity of polystyrene microplastics in lung cells using both mouse and cell culture models. The study found that smaller 1-micrometer particles accumulated more in lung tissue than larger particles and identified epithelial-mesenchymal transition as a key toxic mechanism, driven by ECM-MMP signaling cascades that contribute to lung injury.
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.
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.
Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks
Researchers found that two weeks of oral polystyrene microplastic exposure in ICR mice induced an inflammatory response specifically in the mid colon, suggesting microplastics may contribute to colonic inflammation.
Investigation of pulmonary inflammatory responses following intratracheal instillation of and inhalation exposure to polypropylene microplastics
Rats exposed to polypropylene microplastics through both inhalation and direct lung delivery developed inflammatory responses in their lungs, including increased immune cells and tissue changes. Even at relatively low concentrations, the microplastics triggered pulmonary inflammation, supporting concerns that breathing in airborne microplastics could contribute to respiratory health problems in humans.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers exposed colitis mouse models to polystyrene micro- and nanoplastics to test whether MNP exposure worsens inflammatory bowel disease, finding that MNPs altered biodistribution and exacerbated inflammatory responses in animals with pre-existing gut inflammation.
Potential toxicity of polystyrene microplastic particles
Researchers investigated the cellular-level toxicity of polystyrene microplastic particles and found that they stimulated immune responses in a size- and concentration-dependent manner. The particles triggered the production of cytokines and chemokines, which are signaling molecules involved in inflammation. The study challenges the common assumption that microplastics pose minimal risk to human health, suggesting they may have immunological effects upon direct contact with cells.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
Airborne polystyrene microplastics and nanoplastics induce nasal and lung microbial dysbiosis in mice
Researchers found that airborne polystyrene microplastics and nanoplastics can induce microbial dysbiosis in the nasal passages and lungs of mice. The study showed that both micro- and nanoplastics altered airway microbiota composition, with microplastics having a stronger influence on lung bacterial communities, suggesting that inhaled plastic particles may disrupt respiratory microbial balance.
Inhaled polystyrene nanoparticles may cause fibrotic lesions via immune dysregulation and energy metabolism disturbance
Mice received polystyrene nanoparticles via pharyngeal instillation for 90 days and were assessed for local lung and systemic toxicity. The nanoparticles accumulated in lungs and hearts, caused immune dysregulation, disrupted energy metabolism, and induced fibrotic lesions at higher doses, suggesting that chronic inhalation of nanoplastics may contribute to pulmonary fibrosis.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers studied the effects of polystyrene micro- and nanoplastics in a mouse model of colitis, examining biodistribution, immune cell responses, and gut microbiome changes. The study found that nanosized particles in particular showed distinct biodistribution patterns and affected macrophage polarization under inflammatory conditions, suggesting that intestinal inflammation may alter how the body handles micro- and nanoplastic particles.
Polystyrene nanoplastic exposure enhances LPS-induced lung inflammation in mice by inducing M1 polarization of macrophages via ROS/JAK/STAT signaling pathway
Researchers found that polystyrene nanoplastic exposure in mice enhanced LPS-induced lung inflammation by activating the ROS/JAK2/STAT3 signaling pathway, promoting macrophage M1 polarization over M2, and increasing pro-inflammatory cytokines IL-1beta, TNF-alpha, and IL-6, with JAK2 inhibitor AG490 reversing these effects in both in vivo and in vitro experiments.
Polystyrene microplastic induced airway hyper-responsiveness, and pulmonary inflammation are mitigated by bronchom treatment in murine model of lung disease
Researchers exposed mice to polystyrene microplastics and found that the particles triggered airway hyper-responsiveness, lung inflammation, and structural damage similar to asthma-like symptoms. An herbal medicine called Bronchom, given as a pre-treatment, significantly reduced these harmful effects by lowering inflammatory cell counts and cytokine levels in the lungs. The study suggests that microplastic inhalation can cause meaningful respiratory problems and identifies a potential natural approach for mitigating lung inflammation caused by microplastic exposure.
Inhalation toxicity of polystyrene micro(nano)plastics using modified OECD TG 412
Researchers conducted inhalation toxicity testing of polystyrene micro- and nanoplastics in rats using a modified OECD standard protocol. They found that inhaled plastic particles caused inflammatory responses in lung tissue and were detected in various organs, indicating systemic distribution after inhalation. The study provides important regulatory-relevant data suggesting that airborne microplastics pose measurable inhalation health risks.
Unmodified Polystyrene Nanoparticles Induce Inflammatory and Oxidative Stress Responses in Human Lung Epithelial Cells
Exposure of human lung epithelial cells to unmodified polystyrene nanoparticles (60 nm) at concentrations as low as 50 µg/mL reduced cell viability by about 50% and triggered expression of inflammatory genes including IL-6 and CXCL10. These results suggest that nanoplastic particles reaching the respiratory tract could provoke lung inflammation, raising concerns about the health consequences of inhaling airborne nanoplastics.
Chronic lung tissue deposition of inhaled polyethylene microplastics may lead to fibrotic lesions
In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung
Using a mouse model of mild COVID-19, this study found that microplastic beads co-delivered to the lungs alongside SARS-CoV-2 suppressed early innate immune responses and later amplified pro-inflammatory signals resembling the cytokine release syndrome seen in severe COVID-19 cases. Viral load itself was unchanged, suggesting microplastics do not accelerate infection but instead disrupt the body's ability to regulate inflammation during disease. This raises concern that widespread microplastic inhalation could worsen outcomes during respiratory infections in people already carrying a lung burden of plastic particles.
Pulmonary Toxicity of Polystyrene, Polypropylene, and Polyvinyl Chloride Microplastics in Mice
Researchers tested the lung toxicity of three common microplastic types (polystyrene, polypropylene, and polyvinyl chloride) in mice and found that all three caused pulmonary inflammation, but through different mechanisms. Polyvinyl chloride produced the most severe inflammatory response, while polystyrene and polypropylene showed distinct patterns of immune activation. The study suggests that the type of plastic inhaled matters for understanding respiratory health risks from airborne microplastics.