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Updated: Jan 14, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
Joon Young Choi1, Jung Hur2, Yong Suk Jo2
1Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Background:
Widely 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.
Methods:
Female 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.
Results:
MP 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.
Conclusion:
While MP exposure aggravated inflammatory responses in healthy lungs, it did not exacerbate airway inflammation in asthmatic mice.
Insights
Microplastic (MP) exposure did not worsen asthma in mice. However, it did increase inflammation in healthy lungs, indicating complex respiratory effects.
Area of Science:
- Environmental Science
- Toxicology
- Immunology
Background:
- Microplastics (MPs) are ubiquitous environmental contaminants with potential respiratory health implications.
- Existing research on MPs' role in allergic airway diseases yields inconsistent findings.
- This study examines the immunologic impact of repeated MP exposure in a murine model of ovalbumin (OVA)-induced asthma.
Purpose of the Study:
- To investigate the immunologic effects of repeated microplastic exposure.
- To determine if microplastics exacerbate ovalbumin-induced asthma in a murine model.
Main Methods:
- Female BALB/c mice were divided into control and OVA-sensitized groups, receiving either vehicle or polystyrene MPs intranasally.
- An acute asthma model was induced using ovalbumin sensitization and challenge.
- Lung inflammation was evaluated through bronchoalveolar lavage fluid analysis, histopathology, cytokine profiling, and macrophage polarization assessment.
Main Results:
- Microplastic exposure did not exacerbate allergic airway inflammation in OVA-sensitized mice.
- In OVA-sensitized mice, MPs reduced eosinophil infiltration and levels of IL-5 and IL-13.
- In control mice, MPs increased TNF-α, decreased IFN-γ, upregulated IL-25 and IL-33, and promoted M1 macrophage polarization.
Conclusions:
- Microplastic exposure aggravated inflammatory responses in healthy lungs.
- Microplastics did not exacerbate established airway inflammation in asthmatic mice.
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