Azithromycin Improves Inflammation By Suppressing The Function Of Th17Cells In A Mouse Allergic Asthma Model

Objective:To established the Th17-mediated mouse allergic asthma model withincreased neutriophils around airways,and on the basis of this model,investigate the protective effect of azithromycin on inflammation in thisasthma.Methods:This reaserch established the Th17-mediated mouse allergic asthmamodel with increased neutriophils around airways by sensitization with theOVA and LPS, and then challenge with OVA. Forty eight healthy femaleBALB/c mice were randomly divided into4groups: the control group, theasthma group, the azithromycin group and the dexamethasone group. Themice in the azithromycin group received azithromycin50mg/kg byintraperitoneal injections one hour before the OVA challenge; the mice inthe dexamethasone group received dexamethasone5mg/kg byintraperitoneal injections one hour before the OVA challenge. After that, the following needed to acheive in this experiment:The pathologicchanges of lung tissue were observed by microscope. Non-invasivemeasurements of airway resistance were used to measure allergen-inducedairway hyperresponsiveness (AHR). Total cells and cell proportions inbronchoalveolar lavage fluid (BALF) were observed.The concentrations ofOvalbumin-Specific IgE in serum and IL-17, TNF-, IL-8, IL-5, IFN-inBALF were measured by ELISA.The polarizing levels of the Th1, Th2and Th17cells were detected by Q-PCR.Results:1.Compared with the asthma group, pre-treatment of azithromycinsignificantly abrogated the extent of inflammatory cells infiltration inairway.2. The AHR, total cell number and N%in BALF were significantlydecreased in the azithromycin group (P<0.05).3. Azithromycin down-regulated the expressions of inflammatorycytokines including IL-17, TNF-, IL-8, IL-5in BALF (P<0.05).4. Azithromycin also attenuated the expression of Th17cells in lungtissue (P<0.05).Conclusion:Adoptting OVA and LPS to sensitize mice can activate the Th17cells,so as to establish the asthma model with increased neutriophils aroundairways successfully. Azithromycin pre-treatment has a protective effect on inflammation in this asthma. Whose mechanism may be the inhibitioninflammatory cells infiltration by the reduction Th17differentiation andthe decrease secretion of inflmmtory meditors.