Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice  

作　　者：Kai WANG Hua-hao SHEN Wen LI Hua-qiong HUANG 

机构地区：[1]Department of Respiratory Medicine, the Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310009, China

出　　处：《Acta Pharmacologica Sinica》2007年第11期1791-1796,共6页中国药理学报（英文版）

基　　金：the National Natural Science Foundation of China(№ 30570807);the Natural Science Foundation of Zhejiang Province,China(№ Z303761)

摘　　要：Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.

关 键 词：ASTHMA C-C chemokine INTERLEUKIN-4 lungs inflammation 

分 类 号：R56[医药卫生—呼吸系统]