만성 기관지 천식 마우스 모델에서 항 IgE 항체가 기도염증에 미치는 효과
The Effect of Anti-IgE Antibody on Airway Inflammation in a Mouse Model of Chronic Asthma
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Background: Asthma is a disease characterized by chronic airway inflammation and airway hyperresponsiveness. Immunoglobulin E (IgE) plays a key role in the pathogenesis of allergic diseases and asthma. Recently, nonanaphylactogenic antihuman IgE antibody has been used as a therapeutic agent for asthma. Objective: The present study investigated the effect of anti-IgE antibody on the airway inflammation and hyperresponsiveness (AHR) in a mouse model of chronic asthma. Method: We developed a mouse model of chronic asthma for which ovalbumin (OVA)-sensitized female BALB/c- mice were repeatedly exposed to intranasal OVA administration twice a week for 3 months. Anti-IgE antibodies were intravenously administered starting on the 38th day, he next day after 3 challenges and there after once a month during the intranasal OVA challenge of 3 months. Result: Mice chronically exposed to OVA developed sustained eosinophilic airway inflammation and AHR to methacholine compared with control mice. Treatment with anti-IgE antibody inhibited the development of AHR and eosinophilic inflammation. Moreover, anti-IgE antibody treatment reduced the interleukin-5 and interleukin-13 in bronchoalveolar lavage fluid but did not show the change in interleukin-10 and transforming growth factor-β1 levels. Conclusion: These results suggest that anti-IgE treatment can modulate airway inflammation via regulation of Th2 cytokines.
Abstract
Background: Asthma is a disease characterized by chronic airway inflammation and airway hyperresponsiveness. Immunoglobulin E (IgE) plays a key role in the pathogenesis of allergic diseases and asthma. Recently, nonanaphylactogenic antihuman IgE antibody has been used as a therapeutic agent for asthma. Objective: The present study investigated the effect of anti-IgE antibody on the airway inflammation and hyperresponsiveness (AHR) in a mouse model of chronic asthma. Method: We developed a mouse model of chronic asthma for which ovalbumin (OVA)-sensitized female BALB/c- mice were repeatedly exposed to intranasal OVA administration twice a week for 3 months. Anti-IgE antibodies were intravenously administered starting on the 38th day, he next day after 3 challenges and there after once a month during the intranasal OVA challenge of 3 months. Result: Mice chronically exposed to OVA developed sustained eosinophilic airway inflammation and AHR to methacholine compared with control mice. Treatment with anti-IgE antibody inhibited the development of AHR and eosinophilic inflammation. Moreover, anti-IgE antibody treatment reduced the interleukin-5 and interleukin-13 in bronchoalveolar lavage fluid but did not show the change in interleukin-10 and transforming growth factor-β1 levels. Conclusion: These results suggest that anti-IgE treatment can modulate airway inflammation via regulation of Th2 cytokines.
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