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20 resultsShowing papers similar to Microplastics drives ILC2s function and fatty acid metabolism in allergic airway inflammation via PPARγ signaling
ClearCo-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.
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.
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.
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.
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.
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.
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.
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 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.
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.
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.
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.
Silent invaders: the role of MPs on epithelium inflammation and damage in airway diseases
This review examines how inhaled microplastics and nanoplastics interact with airway epithelial surfaces and trigger inflammatory, oxidative, and structural changes that may contribute to respiratory diseases. The study describes how these particles activate key inflammatory pathways such as NF-kB and PI3K/Akt/mTOR, potentially worsening conditions like asthma and COPD through enhanced barrier dysfunction, oxidative stress, and disrupted tissue repair.
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.
Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis
Researchers fed polystyrene microplastics to mice for six weeks and found that healthy mice developed changes in their colon lining, including altered mucus composition and immune cell populations. When mice with experimentally induced colitis also consumed microplastics, their intestinal inflammation was significantly more severe. The study suggests that microplastic exposure may worsen inflammatory bowel conditions.
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.
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.
Oral exposure to nanoplastics and food allergy in mice fed a normal or high-fat diet
Researchers studied how oral exposure to polystyrene nanoplastics affects food allergy responses in mice fed either a normal or high-fat diet. They found that nanoplastics worsened allergic reactions to a food protein, particularly in mice on the high-fat diet, by increasing gut permeability and shifting immune responses. The study suggests that the combination of nanoplastic exposure and a Western-style diet may be contributing to the rising prevalence of food allergies.
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.
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.