Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma

作     者：Hui-ying WANG Yu DAI Jiao-li WANG Xu-yan YANG Xin-guo JIANG 

作者机构：Department of Allergy the Second Affiliated Hospital School of Medicine Zhejiang University Department of Clinical Laboratory the Second Affiliated Hospital School of Medicine Zhejiang University Department of Respiratory Medicine Hangzhou First People's Hospital Department of Rheumatology and Clinical Immunology the Second Affiliated Hospital School of MedicineZhejiang University Department of Medicine VA Palo Alto Health Care System/Stanford University School of Medicine 

出 版 物：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 (浙江大学学报（英文版）B辑（生物医学与生物技术）)

年 卷 期：2015年第16卷第7期

页      面：622-631页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Project supported by the National Natural Science Foundation of China(No.30600266) the Zhejiang Provincial Science and Technology Project(No.2011C37073) the Zhejiang Provincial Natural Science Foundation(No.LQ12H16012) the National Key Clinical Project of Allergy of China the National Key Clinical Specialist Construction Programs of China 

主　　题：Cluster of differentiation 69(CD69) Eosinophil Interleukin-5(IL-5) Asthma 

摘      要：Objective： Airway inflammation and airway hyper-responsiveness（AHR） are principle pathological manifestations of asthma. Cluster of differentiation 69（CD69） is a well-known co-stimulatory factor associated with the activation, proliferation as well as apoptosis of immune cells. This study aims to examine the effect of anti-CD69 monoclonal antibody（m Ab） on the pathophysiology of a mouse model of asthma. Methods： A murine model of ovalbumin（OVA）-induced allergic airway inflammation was used in this study. Briefly, mice were injected with 20 μg chicken OVA intraperitoneally on Days 0 and 14, followed by aerosol provocation with 1%（0.01 g/ml） OVA on Days 24, 25, and 26. Anti-CD69 m Ab or isotype Ig G was injected intraperitoneally after OVA challenge; dexamethasone（DXM） was administrated either before or after OVA challenge. AHR, mucus production, and eosinophil infiltration in the peribronchial area were examined. The levels of granulocyte-macrophage colony-stimulating factor（GM-CSF） and interleukin-5（IL-5） in bronchoalveolar lavage fluid（BALF） were also assayed as indices of airway inflammation on Day 28 following OVA injection. Results： Pretreatment with DXM together with anti-CD69 m Ab treatment after OVA provocation completely inhibited AHR, eosinophil infiltration and mucus overproduction, and significantly reduced BALF IL-5. However, treatment with DXM alone after OVA challenge only partially inhibited AHR, eosinophil infiltration and mucus overproduction, and did not diminish BALF IL-5. Treatment with either DXM or anti-CD69 m Ab did not alter the concentration of BALF GM-CSF. Conclusions： Anti-CD69 m Ab treatment inhibits established airway inflammation as effectively as DXM pretreatment. This study provides a potential alternative therapeutic opportunity for the clinical management of asthma and its exacerbation.