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61,005 resultsShowing papers similar to 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
ClearCo-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.
Polystyrene nanoplastics aggravate house dust mite induced allergic airway inflammation through EGFR/ERK-dependent lung epithelial barrier dysfunction
In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
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.
Effects of microplastics on allergic airways and potential pathogenesis: a review
This review examines how microplastics, which can enter the body through breathing, eating, and skin contact, may affect allergic airway conditions. Researchers found evidence that microplastics can damage airway lining cells, disrupt the protective barrier of the respiratory tract, and trigger heightened airway reactivity. The study suggests that chronic microplastic exposure may worsen allergic airway inflammation, though more research is needed to fully understand the mechanisms involved.
Co-exposure to microplastics enhances the allergenic potentials of house dust mite allergen Der p 1
This study found that polystyrene microplastics can make common house dust mite allergens more potent, increasing allergic reactions. The microplastics changed the shape of the allergen protein, boosting its ability to trigger immune responses and worsening airway inflammation in mice. This research suggests that indoor microplastic pollution could be contributing to the rising rates of allergies and asthma by making existing allergens more harmful.
Cellular and molecular mechanisms of allergic asthma
Researchers reviewed the cellular and molecular mechanisms behind allergic asthma, finding that rising exposure to environmental pollutants — including microplastics — likely contributes to the disease's increasing prevalence, as pollutants disrupt airway barrier integrity and trigger immune responses that lead to chronic airway inflammation.
Microplastics drives ILC2s function and fatty acid metabolism in allergic airway inflammation via PPARγ signaling
Researchers found that microplastics exacerbate allergic airway inflammation in house dust mite-sensitized mice by promoting epithelial barrier disruption and type 2 immune activation. The study revealed that microplastics drive the function of innate lymphoid cells (ILC2s) and alter fatty acid metabolism through the PPARgamma signaling pathway, providing mechanistic insight into how airborne microplastics may worsen respiratory allergies.
Airway exposure to microplastics: Potential mechanisms from epithelial barrier damage to the development of allergic rhinitis
This review summarized the mechanisms by which airborne microplastic exposure triggers allergic rhinitis, identifying pathways including physical and chemical disruption of the airway epithelial barrier, oxidative stress from adsorbed pollutants, and induction of Th2 immune responses and IgE class-switching. The findings support airborne MPs as a novel trigger for upper respiratory allergic disease.
The Impact of Microplastics on Allergy: Current Status and Future Research Directions
This study reviews current evidence on how microplastics may influence allergic responses, noting that microplastics can compromise epithelial barriers and promote type 2 inflammation associated with allergies. The authors emphasize an urgent need for research into dose-dependent immunotoxicological mechanisms to better understand the relationship between microplastic exposure and allergy development. The study calls for evidence-based policies to reduce microplastic exposure and its potential contribution to the growing allergy burden.
Combined exposure to microplastics and particulate matter induced intestinal inflammation and barrier dysfunction
Researchers established a mouse model combining daily microplastic ingestion and particulate matter inhalation to simulate combined water and air pollution exposure. They found that combined exposure induced greater intestinal inflammation, barrier dysfunction, and gut dysbiosis than either pollutant alone.
Co-exposure of polystyrene nanoplastics and ozone synergistically induced airway inflammation: Evidence and biomarkers screening
Researchers discovered that co-exposure to airborne polystyrene nanoplastics and ozone in mice caused significantly worse airway inflammation than either pollutant alone, with the two acting synergistically. They identified specific metabolic pathways and genes involved in the inflammatory response, providing potential biomarkers for monitoring this type of combined exposure. The findings suggest that breathing in nanoplastics alongside common air pollutants like ozone may pose amplified respiratory health risks.
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.
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.
Progress in understanding the impact of microplastics on respiratory allergic diseases
This review synthesized evidence on how airborne microplastics may affect respiratory allergic diseases such as allergic rhinitis and asthma. Researchers found that inhaled microplastics can compromise airway barriers by disrupting tight junctions, impairing mucus clearance, and weakening mucosal defenses. The study suggests that microplastic characteristics like polymer type, particle size, and surface chemistry influence how they initiate or worsen respiratory allergic responses.
Evidence that microplastics aggravate the toxicity of organophosphorus flame retardants in mice (Mus musculus)
Researchers co-exposed mice to polyethylene and polystyrene microplastics along with organophosphorus flame retardants for 90 days and found that microplastics aggravated the toxicity of the flame retardants. Evidence from biochemical markers and metabolomics indicated increased oxidative stress and metabolic disruption in co-exposed animals, suggesting microplastics may worsen the health effects of chemical pollutants they encounter in the environment.
Microplastics in Allergic Rhinitis: Multimechanistic Drivers of Barrier Disruption and Immune Dysregulation
This review examines the multimechanistic pathways by which microplastics drive barrier disruption and immune dysregulation in allergic rhinitis, considering how physical and chemical properties of microplastic particles interact with nasal epithelial and immune function. The paper synthesizes emerging evidence on microplastics as a novel contributor to upper airway allergic disease.
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.
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.
Presence of nanoplastics in sputum of patients with severe asthma: a novel environmental perspective
Researchers analyzed sputum from severe asthma patients and detected nanoplastics in samples for the first time, comparing concentrations and immune profiles across asthma phenotypes. Nanoplastic presence in sputum was associated with more severe disease and distinct immune dysregulation patterns, identifying environmental nanoplastic exposure as a potential modifier of asthma severity.
In vivo toxicity assessment of microplastics in Balb/C mice : study of inhalation exposure and its inflammatory effects
Researchers examined the in vivo toxicity of inhaled microplastics in Balb/C mice, studying pulmonary inflammation, oxidative stress, and systemic effects following repeated inhalation exposure. The study found dose-dependent lung inflammation and evidence of particle translocation to other organs.
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.
Detection of microplastics in patients with allergic rhinitis
In a study of 66 patients, researchers found significantly more microplastic particles in nasal wash samples from people with allergic rhinitis compared to healthy volunteers. The microplastics found were mostly fibers and fragments small enough to deposit in nasal passages during normal breathing. This is among the first studies to link airborne microplastic exposure in the nose to an allergic condition, suggesting inhaled microplastics may contribute to nasal inflammation.
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.