Effects of type-3-polysaccharide on airway inflammation and Treg/Th17 cells in bronchial asthmatic mice
Luo Yong-ai
Abstract
Luo Yong-ai
Abstract
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 RORyt 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 OVA-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(P0.05).The BALF levels of IFN-γand 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(P0.05),while RORyt mRNA expression and the proportion of Th17 cells among CD4~+ cells were significantly lower than in the asthma group(P0.05). The count of BALF eosinophils was negatively correlated with the ratios of Foxp3-mRNA/RORγt-mRNA and Treg/Th17 in asthma and T3P groups(P0.05).Conclusion T3P may inhibit airway inflammation by inhibiting OVA-IgE and regulating Thl/Th2 and Treg/Th17 cell balance in asthmatic mouse model.
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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 RORyt 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 OVA-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(P0.05).The BALF levels of IFN-γand 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(P0.05),while RORyt mRNA expression and the proportion of Th17 cells among CD4~+ cells were significantly lower than in the asthma group(P0.05). The count of BALF eosinophils was negatively correlated with the ratios of Foxp3-mRNA/RORγt-mRNA and Treg/Th17 in asthma and T3P groups(P0.05).Conclusion T3P may inhibit airway inflammation by inhibiting OVA-IgE and regulating Thl/Th2 and Treg/Th17 cell balance in asthmatic mouse model.
Key concepts: FOXP3, Ovalbumin, Bronchoalveolar lavage, Immunoglobulin E, Immunology, Asthma, Inflammation, Allergic inflammation