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 t...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.展开更多
基金Project supported by the National Natural Science Foundation of China(No.30600266)the Zhejiang Provincial Science and Technology Project(No.2011C37073)+2 种基金the Zhejiang Provincial Natural Science Foundation(No.LQ12H16012)the National Key Clinical Project of Allergy of Chinathe National Key Clinical Specialist Construction Programs of China
文摘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.
