Objective      To determine the effect of azithromycin on the inflammation in Th17-mediated mouse allergic asthma model with increased neutrophils around airways.       Methods      Th17-mediated mouse allergic asthma model with increased neutrophils around airways was established by sensitization with ovalbumin (OVA) and LPS

and challenge with OVA. Forty-eight healthy female BALB/c mice were randomly divided into 4 groups

control

asthma group

azithromycin group and dexamethasone group. Pathologic changes of lung tissue were observed by microscopy. Non-invasive measurements of airway resistance were used to measure allergen-induced airway hyperreactivity (AHR).Total cells and cell proportions in bronchoalveolar lavage fluid (BALF) were observed. The concentrations of OVA-specific IgE in the serum and of IL-17

TNF-α

IL-8

IL-5

and TNF-γ in the BALF were measured by ELISA. The polarizing levels of the Th1

Th2 and Th17 cells were detected by Q-PCR.       Results      Combining OVA and LPS could establish a mouse model of allergic asthma with Th2 activation and eosinophils increase in the lung

and simultaneously

enhanced Th17 expression and apparent neutrophilic inflammation. Compared with the asthma group

azithromycin attenuated inflammatory cells infiltration in airway

and decreased N% significantly (P0.05). Moreover

the levels of IL-17

TNF-α

IL-8

and IL-5 in the BALF were reduced in azithromycin treated group (P0.05). In addition

azithromycin effectively attenuated Th17 cells differentiation in lung tissue (P0.05) and reduced AHR (P0.05). However

in the dexamethasone group

even though E% in the BALF was reduced significantly compared to asthma group

there was no significant difference between the dexamethasone group and asthma group in total cell number

levels of IL-17

TNF-α

and IL-8 in the BALF and differentiation of Th17 cells in lung tissue (P0.05).       Conclusion      Azithromycin can attenuate inflammation in Th17-mediated mouse allergic asthma model with increased neutrophils around airways. The underlying mechanism may be the inhibition of inflammatory cells infiltration by reducing Th17 differentiation and decreasing secretion of inflammatory mediators.