ArticleTuberculosis and respiratory diseases2026
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model.
Article in Tuberculosis and respiratory diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Micro- and Nanoplastics as Environmental Stressors: Mechanistic Links Among Gut Dysbiosis, Inflammation, and Systemic Health Effects.Journal of xenobiotics · 2026Review
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Authors and funding
4 authors.
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Abstract
backgroundWidely distributed in the environment, microplastics (MPs) are increasingly recognized as potential respiratory hazards. While several studies suggest their role in worsening allergic airway diseases, findings remain inconsistent. This study aimed to investigate the immunologic effects of repeated MP exposure in an acute murine model of ovalbumin (OVA)-induced asthma.
methodsFemale BALB/c mice were assigned to four groups: control with vehicle, control with MPs, OVA-sensitized with vehicle, and OVA-sensitized with MPs. An acute asthma model was established by sensitizing and challenging mice with OVA. Spherical polystyrene MPs of 1-5 μm were administered intranasally at 300 μg daily from day 0 to 21. Lung inflammation was assessed via bronchoalveolar lavage fluid (BALF) analysis, histopathology, cytokine measurements, and macrophage polarization by immunofluorescence.
resultsMP exposure did not exacerbate allergic inflammation in OVA-sensitized mice. Instead, it led to reduced eosinophilic infiltration and lower levels of interleukin 5 (IL-5) and IL-13, compared to vehicle-treated OVA mice. In contrast, MP exposure in control mice increased tumor necrosis factor-α and decreased interferon-γ levels, upregulated epithelial alarmins (IL-25 and IL-33), and elevated inflammation scores. Alarmin levels, including IL-25 and IL-33, were elevated by MP exposure in control mice, whereas no significant differences were observed between vehicle- and MP-treated mice in the OVA-sensitized group. Macrophage analysis showed a shift toward M1 polarization only in control mice.
conclusionWhile MP exposure aggravated inflammatory responses in healthy lungs, it did not exacerbate airway inflammation in asthmatic mice.
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