RESUMO
Objective To investigate the effects of type-3-polysaccharide (T3P) on airway inflammation and Treg/Th17 cells in bronchial asthmatic mice. so as to explore the immunoregulation mechanism of T3P in asthmatic mice. Methods BALB/c mice were randomly divided into 3 groups, with 8 mice in each group. The control group received PBS treatment, the asthma group were sensitized and challenged with ovalbumin(OVA),and the T3P group received a pretreatment with T3P by subcutaneous injection before sensitization with OVA. The pulmonary histological changes were observed and differential cell counts in bronchoalveolar lavage fluid (BALF) were performed. Serum OVA-IgE and IFN-γ IL-4, IL-17 and IL-10 levels in the BALF were detected by enzyme-linked immunosorbent assay (ELISA). The levels of Foxp3 and RORγt mRNA expression were measured by real-time fluorescence-based quantitative PCR. The proportions of Treg and Th17 cells in CD4+cells were assessed by flow cytometric analysis. Results The inflammatory degree of pulmonary tissue, serum OV-IgE, and total cell number, proportion of eosinophils, and IL-4, IL-17 levels in BALF were significantly lower in T3P group than in the asthma group (P<0. 05). TheBALF levels of IFN-y and IL-10, Foxp3 mRNA expression and proportion of Treg cells among CD4+ cells were significantly higher in the T3P group than in the asthma group (P<0. 05), while RORut mRNA expression and the proportion of Th17 cells among CD4+ cells were significantly lower than in the asthma group (P<0. 05). The count of BALFeosinophils was negatively correlated with the ratios of Foxp3-mRNA/RORut~mRNA and Treg/Th17 in asthma and T3P groups (P<0. 05). Conclusion T3P may inhibit airway inflammation by inhibiting OVA-IgEand regulating Th1/Th2 and Treg/Th17 cell balance in asthmatic mouse model.