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Updated: Jul 7, 2025
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Establishment of a juvenile mouse asthma model induced by postnatal hyperoxia exposure combined with early OVA
Jingyan Li1, Tianping Bao1, Linxia Cao1
1Department of Neonatology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai 'an, Jiangsu, 223300, China.
Insights
This study developed a juvenile mouse asthma model using hyperoxia and ovalbumin (OVA) sensitization. The model effectively mimicked asthma symptoms, showing increased airway hyperreactivity and inflammatory markers.
Area of Science:
- Pediatric Respiratory Research
- Animal Models of Disease
- Immunology
Background:
- Asthma is a chronic respiratory disease affecting children worldwide.
- Developing reliable juvenile asthma models is crucial for research.
- Postnatal environmental factors may influence asthma development.
Purpose of the Study:
- To establish a juvenile mouse model of asthma.
- To investigate the effects of postnatal hyperoxia and ovalbumin (OVA) sensitization.
Main Methods:
- Newborn mice were exposed to hyperoxia (95% O2) and sensitized with OVA.
- Airway responsiveness (AHR), lung pathology, and inflammatory markers (IL-5, IL-13, IL-17A, IgE) were assessed.
- Groups included room air (RA)+PBS, O2+PBS, RA+OVA, and O2+OVA.
Main Results:
- The O2+OVA group exhibited asthma-like symptoms and increased AHR.
- Elevated levels of IL-5, IL-13, IL-17A, total IgE, and specific IgE were observed.
- Significant increases in total leukocytes and eosinophils were noted in BALF.
Conclusions:
- Postnatal hyperoxia combined with early OVA sensitization successfully established a juvenile mouse asthma model.
- This model demonstrates key features of asthma, including airway hyperreactivity and inflammation.
- The model provides a valuable tool for studying pediatric asthma pathogenesis and treatment.
Objective:
To establish a juvenile mouse asthma model by postnatal hyperoxia exposure combined with early ovalbumin (OVA) sensitization.
Methods:
Female C57BL/6J newborn mice were exposed to hyperoxia (95 % O2) from postnatal day-1 (PND1) to PND7; intraperitoneally injected with OVA suspension on PND21, PND28; and stimulated by nebulized inhalation of 1 % OVA from PND36 to PND42. Within 48 h of the last challenge, we observed their activity performance and evaluated airway responsiveness (AHR). All mice were executed at PND44. Female (n = 32) were divided into four groups as follows: room air（RA）+phosphate-buffered saline (PBS) group; O2 (hyperoxia, 95 % O2) + PBS group; RA + OVA group; O2+OVA group. We obtained the serum, bronchoalveolar lavage fluid (BALF), and lung tissues. The Wright-Giemsa staining was performed for leukocyte classification in BALF and HE staining for pathological examination. The levels of IL-2, IL-5, IL-13, IL-17A and IL-10 in BALF and tIgE and sIgE in serum were detected by ELISA.
Results:
Compared with OVA sensitization or hyperoxia exposure alone, the mice in the model group (O2+OVA) showed asthma-like symptoms and increased airway hyperreactivity,The levels of IL-5,IL-13 IL-17A were increased in BLAF,and total leukocyte and eosinophil counts were also significant increasesed. The levels of tIgE and sIgE in serum were increased.
Conclusion:
Postnatal hyperoxia exposure combined with early OVA sensitization might establish a juvenile mouse asthma model.
