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

来源 :Acta Pharmacologica Sinica | 被引量 : 0次 | 上传用户:tuojing
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Aim:To evaluate the effect of C-C chemokine receptor 3 (CCR3) blockade onpulmonary inflammation and mucus production in allergic mice.Methods:Weused the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigenand generated murine monoclonal antibody against the human CCR3.In addition,the generated antibody was administered to mice sensitized and challenged withovalbumin.The inflammatory cells in bronchoalveolar lavage,cytokine levels,pulmonary histopathology,and mucus secretion were examined.Results:TheWestern blotting analysis indicated that the generated antibody bound to CCR3specifically.The allergic mice treated with the antihuman CCR3 antibody exhib-ited a significant reduction of pulmonary inflammation accompanied with the al-teration of cytokine.Conclusion:The antibody we generated was specific toCCR3.The inhibition of airway inflammation and mucus overproduction by theantibody suggested that the blockade of CCR3 is an appealing therapeutical tar-get for asthma.The present research may provide an experimental basis for thefurther study of this agent. Aim: To evaluate the effect of CC 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. 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 CCR3specifically.The allergic mice treated with the antihuman CCR3 antibody exhib- ited a significant reduction of pulmonary inflammation accompanied with the al-teration of cytokine. Conlusion: The antibody we generated was specific to CCR3. inhibition by airway inflammation and mucus overproduction by the antibody said that the blockade of CCR3 is an appealing therapeutical tar-get for asthma. p resent research may provide an experimental basis for the further study of this agent.
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