| The effects of early allergen/endotoxin exposure on subsequent
allergic airway inflammation to allergen in mouse model of asthma |
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Yeong-Ho Rha, Sun-Hee Choi |
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Departement of Pediatrics, School of Medicine, Kyunghee University, Seoul, Korea |
| 생쥐 천식모델에서 생후 조기 알레르겐/내독소 노출이 성숙 후 알레르기 기도염증에 미치는 영향 |
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나영호, 최선희 |
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경희대학교 의과대학 소아과학교실 |
Correspondence:
Yeong-Ho Rha, Email: yhrha@khu.ac.kr
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| Abstract |
Purpose
: Recently many studies show early exposure during childhood growth to endotoxin (lipopolysaccharides, LPS) and/or early exposure to allergens exhibit important role in development of allergy including bronchial asthma. The aim
of this study was to evaluate the role of endotoxin and allergen exposure in early life via the airways in the pathogenesis of allergic airways inflammation and airway hyperresposiveness (AHR) in mouse model of asthma.
Methods
: Less than one week-old Balb/c mice was used. Groups of mice were received either a single intranasal instillation of sterile physiologic saline, 1% ovalbumin (OVA), LPS or 1.0 μg LPS in 1% OVA. On 35th day, these animals were sensitized
with 1% OVA for 10 consecutive days via the airways. Animals were challenged with ovalbumin for 3 days on 55th days, and airway inflammation, hyperresponsiveness, and cytokine expression were assessed. Measurements of airway
function were obtained in unrestrained animals, using whole-body plethysmography. Airway responsiveness was expressed
in terms of % enhanced pause (Penh) increase from baseline to aerosolized methacholine. Lung eosinophilia, serum
OVA-IgE and bronchoalveolar lavage (BAL) fluid cytokine levels were also assessed. ANOVA was used to determine the levels of difference between all groups. Comparisons for all pairs were performed by Tukey-Kramer honest significant difference test; P values for significance were set to 0.05.
Results
: Sensitized and challenged mice with OVA showed significant airway eosinophilia and heightened responsiveness to methacholine. Early life exposure of OVA and/or LPS via the airway prevented both development of AHR as well as bronchoalveolar lavage fluid eosinophilia. Exposure with OVA or LPS also resulted in suppression of interleukin (IL)-4, 5 production in BAL fluid and OVA specific IgE in blood.
Conclusion
: These results indicate that antigen and/or LPS exposure in the early life results in inhibition of allergic responses to OVA in this mouse model of astham. Our data show that early life exposure with OVA and/or LPS may have a protective role in the development of allergic airway inflammation and development of allergen-induced airway responses in mouse model of asthma. |
| Key Words:
Asthma model, Mouse, Endotoxin, Ovalbumin |
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