论文部分内容阅读
目的:气道慢性炎症和高反应性是哮喘最主要的病理生理表现,CD69是一种与免疫细胞活化、增殖及凋亡密切相关的共刺激分子,本研究旨在观察抗CD69单克隆抗体在哮喘小鼠模型中抑制气道炎症和高反应性的作用及机制探讨。创新点:(1)与大多数关于哮喘的药物研究多为造模前提前用药以阻断炎症的进展相比,本研究将抗CD69单抗作用于气道已经形成的炎症,与临床上哮喘的治疗更接近;(2)抗CD69单抗的独特作用在于它特异性地作用于气道活化的炎症细胞,与已有的哮喘药物以糖皮质激素相比,可能的全身反应少。方法:鸡卵白蛋白致敏激发制备哮喘模型(图1),Buxco系统测试哮喘小鼠的气道高反应性(图6)。结论:抗CD69单克隆抗体可抑制哮喘小鼠已经形成的气道炎症,其作用效果与地塞米松预处理相当。本研究为临床哮喘的急性发作治疗和管理提供了新的可能靶点。
OBJECTIVE: Chronic inflammation and hyperresponsiveness of the airways are the most important pathophysiological manifestations of asthma. CD69 is a co-stimulatory molecule closely related to the activation, proliferation and apoptosis of immune cells. The purpose of this study was to investigate the effect of anti-CD69 monoclonal antibody Role and Mechanism of Inhibiting Airway Inflammation and Hyperresponsiveness in Asthmatic Mouse Model. Innovative point: (1) Compared with the majority of drug research on asthma and premedication to block the progress of inflammation in advance compared to the anti-CD69 monoclonal antibody in the airway has been the formation of inflammation, and clinical asthma (2) The unique effect of the anti-CD69 mAb is that it acts specifically on airway-activated inflammatory cells with less likely systemic reactions than existing asthma drugs, glucocorticoid. Methods: Asthmatic models were prepared with chicken ovalbumin challenge (Figure 1) and the Buxco system was used to test airway hyperresponsiveness in asthmatic mice (Figure 6). Conclusion: The anti-CD69 monoclonal antibody can inhibit the airway inflammation in asthmatic mice and its effect is comparable to dexamethasone pretreatment. This study provides new possible targets for the treatment and management of acute attacks of clinical asthma.