Objective      To observe the expression of CC chemokine ligand 20 (CCL20) in the lung tissues of asthmatic mice and the effect of anti-CCL20 monoclonal antibody on airway inflammation and airway hyper-responsiveness (AHR) in asthmatic BALB/c mice.       Methods      A total of 32 BALB/c mice at the age of 6 to 8 weeks were randomly divided into an asthma group

a no

rmal control group

an anti-CCL20 monoclonal antibody treatment group and a therapeutic control group. The mice in the asthma group were sensitized and challenged with ovalbumin (OVA) to establish an asthma model

while the mice in the normal control group were sensitized and challenged with PBS. The sensitive and challenge methods of the anti-CCL20 monoclonal antibody treatment group and the therapeutic control group were the same as that of the asthma group. But since the first challenge

mice of the former 2 groups received an intraperitoneal injection of anti-CCL20 monoclonal antibody and PBS

respectively

in 1 h before atomization inhalation for 5 consecutive days. Within 24 h after the final OVA challenge

AHR was measured by lung function instrument. The degree of  inflammation in lung tissue was evaluated by HE staining. The expression of CCL20 at mRNA and protein levels in lung tissue were detected by real-time fluorescent quantitative PCR (real-time PCR) and immunochemistry assay.       Results      Compared with the normal control group

the score of inflammation in lung tissue

the AHR

the expression of CCL20 mRNA in lung tissue homogenate and the mean density for CCL20 of the asthma group were significantly higher. In the anti-CCL20 monoclonal antibody treatment group

pulmonary cell infiltration was alleviated when compared with the asthma group (

P

0.05). Lung function Penh values were significant lower in the anti-CCL20 monoclonal antibody treatment group than in the asthma group (

P

0.05). The mean density for CCL20 was significant lower in the anti-CCL20 monoclonal antibody treatment group than in the asthma group (

P

0.01)

but the CCL20 mRNA expression showed no obvious difference among the groups.       Conclusion      Anti-CCL20 monoclonal antibody can attenuate OVA-induced mice asthma inflammation and AHR

possibly involving CCL20 activity blockage by the antibody.