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.

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