动物造模,支气管哮喘转基因动物模型 z-bio 2021-03-25 716

　　(1) The replication method mainly uses transgene or gene knockout technology to study the role of changes in specific gene expression products in the development of asthma.

　　(2) Model characteristics

　　1) The transcription factor GATA-3 transgenic mouse IL-4, IL-5, and interleukin 13 (IL-13) synthesis model is reduced, the airway EOS produces sensitized infiltration, stimulates mucus secretion, and significantly reduces IgE synthesis. GATA-3 regulates the expression of Th2 cytokines, and the elimination of GATA-3 activity may slow down the response of Th2 cells, making it a new target for asthma treatment. 2) CD23 transgene and knockout mouse anti-CD23 antibodies can inhibit the synthesis of IgE and IgG1 in the OVA-induced Balc/c mouse asthma model, and prevent the penetration of EOS and the production of AHR in the lung. However, the degree of EOS infiltration and airway hyperresponsiveness induced by sensitization in CD23 transgenic mice was significantly negatively correlated with the expression of CD23 on T cells and B cells. CD23-/- (knockout) mice are more likely to cause asthma symptoms than CD23 ++/+ mice, and CD23 can not only promote the development of asthma, but also has a negative regulatory effect on allergic reactions and AHR, which indicates the existence of sexual behavior.

　　(3) Comparative medicine Bronchial asthma is a chronic airway inflammation that involves eosinophils (EOS), mast cells, T lymphocytes and other inflammatory cells, leading to airway hyperresponsiveness (AHR) in patients and airways, leading to Obstruction and restricted airflow. The causes of bronchial asthma are complex, and the limitations of direct human studies need to be considered to identify the cause, investigate the cause, evaluate new therapies, and research and develop new drugs. Therefore, establishing an animal model of bronchial asthma provides a tool for further research.