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

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.