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61,005 resultsShowing papers similar to Mechanisms underlying Th2-dominant pneumonia caused by plastic pollution derivatives (PPD): A molecular toxicology investigation that encompasses gut microbiomics and lung metabolomics
ClearMechanisms 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.
Gut-lung axis: a novel mechanism involving microbiota dysbiosis-coordinated PLA2-TRPV1 neuroimmune crosstalk in nanoplastic-induced asthma exacerbation
Researchers found that inhaled polystyrene nanoplastics worsen asthma in mice by triggering a chain reaction involving gut bacteria disruption, nerve-immune signaling, and airway inflammation, revealing a gut-lung connection where plastic particles in the body can amplify respiratory disease through multiple biological pathways at once.
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.
Gut-lung microbiota dynamics in mice exposed to Nanoplastics
Researchers gave mice PET nanoplastics orally for 28 days and analyzed the microbiome in their lungs, colon, mouth, and stool. While gut and oral bacteria were relatively unchanged, the lung microbiome showed significant shifts, including increases in bacteria associated with respiratory inflammation. The findings suggest a gut-lung connection where ingested nanoplastics may influence lung microbial communities even when gut bacteria appear unaffected.
Effects of secondary microplastic on the respiratory system of BALB/c mice
Researchers exposed BALB/c mice to secondary microplastics derived from environmentally weathered plastic and assessed respiratory system effects. Secondary MPs caused greater pulmonary inflammation and oxidative stress than virgin particles, suggesting that real-world aged plastics carry higher respiratory toxicity risks than pristine particles used in most laboratory studies.
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.
Harmful effects of true-to-life nanoplastics derived from PET water bottles in human alveolar macrophages.
Researchers tested nanoplastics derived from actual PET water bottles on mouse lung immune cells, focusing specifically on cells that had internalized the particles. Even though the nanoplastics were taken up by 100% of cells at the highest dose, they did not cause outright cell death. However, they did trigger significant increases in reactive oxygen species and shifted the immune cells toward a pro-inflammatory state, suggesting that inhaled nanoplastics from everyday plastic products could promote chronic lung inflammation.
Synergistic pulmonary toxicity of resorcinol bis(diphenylphosphate) and microplastics: Integrated proteomics and metabolomics approach reveals oxidative stress-inflammatory crosstalk
Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
Pulmonary Flora‐Derived Lipopolysaccharide Mediates Lung‐Brain Axis through Activating Microglia Involved in Polystyrene Microplastic‐Induced Cognitive Dysfunction
In a mouse study, inhaling polystyrene microplastics impaired learning and memory -- even though the plastics never reached the brain directly. Instead, the microplastics changed the bacterial community in the lungs, which produced inflammatory signals that traveled to the brain and triggered damage, revealing a lung-to-brain pathway for microplastic harm.
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.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
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.
Co-exposure to polystyrene microplastics and di-(2-ethylhexyl) phthalate aggravates allergic asthma through the TRPA1-p38 MAPK pathway
This mouse study found that polystyrene microplastics combined with DEHP, a common plastic additive, worsened allergic asthma symptoms more than either pollutant alone. The combination activated an inflammatory pathway called TRPA1-p38 MAPK in lung tissue, increasing airway inflammation and mucus production. The findings suggest that real-world exposure to microplastics carrying chemical additives could aggravate respiratory conditions like asthma.
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.
Unveiling the systemic impact of airborne microplastics: Integrating breathomics and machine learning with dual-tissue transcriptomics
Researchers developed a new non-invasive way to detect microplastic damage in mice by analyzing chemicals in their breath. When mice inhaled tiny polystyrene particles, the plastics caused inflammation in their lungs and injury to their hearts, with specific breath chemicals serving as warning signs. This approach could eventually help doctors detect microplastic-related health problems in people through a simple breath test.
Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective
This review examines immunometabolic reprogramming mechanisms in sepsis-associated acute respiratory distress syndrome from the perspective of the gut-lung axis. While not directly about microplastics, the research explores immune pathways and gut-lung interactions that are relevant to understanding how environmental pollutants including microplastics may affect inflammatory responses. The study provides context on the biological mechanisms through which gut-derived signals can influence lung inflammation and immune cell function.
Exposure to environmental xenobiotics and lung tissue function: A comprehensive review on biological mechanisms and pathways
This comprehensive review examines how environmental pollutants including microplastics, heavy metals, and volatile organic compounds damage lung tissue through mechanisms like oxidative stress, inflammation, and disruption of cellular barriers. The study suggests these pollutants contribute to chronic respiratory diseases and highlights how they can also cause epigenetic changes that may affect future generations.
Inhaled microplastics and lung health: Immunopathological effects and disease implications
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.
Sub-acute polyethylene microplastic inhalation exposure induced pulmonary toxicity in wistar rats through inflammation and oxidative stress
Researchers exposed rats to airborne polyethylene microplastics through inhalation for 28 days and found significant signs of lung damage. The exposed animals showed increased inflammation markers, elevated oxidative stress, and tissue changes in the lungs compared to controls. The study provides evidence that breathing in microplastic particles from degraded plastic bags and bottles may cause pulmonary toxicity.
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.
Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via CXCL1 signaling pathway in a mouse model
In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
Lung microbiota participated in fibrous microplastics (MPs) aggravating OVA-induced asthma disease in mice
In a mouse study, inhaling fiber-shaped microplastics significantly worsened asthma symptoms, including airway inflammation, mucus buildup, and lung tissue scarring. The microplastic fibers also disrupted the balance of bacteria living in the lungs and activated inflammatory pathways. Since fibrous microplastics are the most common airborne shape and have been found in human lungs, this research suggests they could worsen respiratory conditions like asthma in people.
Short-term microplastic exposure: A double whammy to lung metabolism and fecal microflora in diabetic SD rats
Researchers studied the effects of short-term polystyrene microplastic exposure on diabetic rats and found that the particles caused lung tissue damage and significant changes to gut bacteria composition. The microplastic exposure disrupted metabolic processes in the lungs and altered the balance of beneficial and harmful microbes in the gut. The findings suggest that individuals with diabetes may be particularly vulnerable to the health effects of microplastic exposure, even at low doses over short periods.
Inhaled 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.