title: Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma.
abstract: 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 (mAb) 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 mAb or isotype IgG 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 mAb 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 mAb did not alter the concentration of BALF GM-CSF.
  
  
  CONCLUSIONS
  Anti-CD69 mAb 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.
authors.affiliation: Department of Allergy, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; Department of Clinical Laboratory, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; Department of Respiratory Medicine, Hangzhou First People's Hospital, Hangzhou 310006, China; Department of Rheumatology and Clinical Immunology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; Department of Medicine, VA Palo Alto Health Care System/Stanford University School of Medicine, Stanford, CA 94305, USA.
authors.forename: Hui-ying
authors.initials: HY
authors.lastname: Wang
authors.forename: Yu
authors.initials: Y
authors.lastname: Dai
authors.forename: Jiao-li
authors.initials: JL
authors.lastname: Wang
authors.forename: Xu-yan
authors.initials: XY
authors.lastname: Yang
authors.forename: Xin-guo
authors.initials: XG
authors.lastname: Jiang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D003907:Dexamethasone / Q000008:administration & dosage; D004359:Drug Therapy, Combination / Q000379:methods; D037181:Lectins, C-Type / Q000037:antagonists & inhibitors / Q000276:immunology*; D051379:Mice; D011014:Pneumonia / Q000276:immunology* / Q000517:prevention & control*; D016896:Treatment Outcome; D000099192:CD69 Antigens
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016207:Cytokines; D003907:Dexamethasone; D037181:Lectins, C-Type; D000099192:CD69 Antigens
keywords: Asthma; Cluster of differentiation 69 (CD69); Eosinophil; Interleukin-5 (IL-5)