| Objective: To establish a mice model of smoke-induced pulmonary emphysema and fibrosis , on which the investigation of the role of CD4+CD25+ regulatory T cell in the the pathogenesis of pulmonary emphysema and fibrosis could be based.Methods: Twenty-four mice were randomly grouped into the smoke exprosure group (group A), the pentoxifylline treated group (group B) and the control group (group C). Mice in group A and group B had been exposed to smoke for 4 months , while the mice in group C which had been raised in the same condition as that in group A and B received no specific interventions. Pulmonary slices were stained by hematoxylin and eosin (HE)and Masson. The mean linear intercepts (Lm) as an index of pulmonary emphysema was used for quantitative analysis of the severity of emphysema. The degree of alveolitis and interstitial fibrosis were evaluated according to Maeyama's theory. The content of hydroproline in the homogenate of lung specimens are measured by spectrophotograhy analysis.Results: The lungs sequestered from group A mice manifested similar pathological changes to pulmonary emphysema, as shown by HE and Masson staining. And the Lm value, as a measure of interalveolar wall distance, was significantly greater in the mice of group A as compared to the two other groups (P<0.05). In group B, the total output suggested a trend towards pulmonary fibrosis, as the difference of the content of hydroproline in the homogenate of lung tissues among the three groups is statistically significant.Conclusions: Based on long-term tobacco smoke inhalation, a mice model of smoke-induced pulmonary emphysema and fibrosis could be established, which set a valid basis for us to further digging into the role of CD4+CD25+ regulatory T cell in the pathogenesis of pulmonary emphysema and fibrosis.PARTⅡThe role of CD4+CD25+ regulatory T cell in the pathogenesis of smoke-induced pulmonary emphysema and fibrosisObjectives: To elucidate the role of Th1/Th2 polarization and CD4+CD25+ regulatory T cell in the pathogenesis of smoke-induced pulmonary emphysema and fibrosis.Methods: Mice in each group were lavaged to collect the bronchoalveolar lavage fluid(BALF), of which the cells were counted and categorized,and the concentration of IFN-γand IL-13 were detected. The concentrations of IL-10 in the homogenate of lung samples were detected by enzyme-linked immunosorbent assay(ELISA). The monocellular suspension of mice spleen was prepared to detect by flow cytometry the proportion of CD4+CD25+ regulatory T cell in CD4+ cells. The data were analyzed using SPSS11.5.Results: The cell counts in the BALF of emphysema group and the fibrosis group mice are significantly higher than that in the control group(P<0.01,both). The counts of neutrophils and macrophages in the BALF of emphysema group mice are significantly higher than in the control group(P<0.05), the count of neutrophils and lymphocytes in the BALF of fibrosis group is significantly higher than than that in the control group(P<0.01,both). The concentration of IFN-γin the BALF of emphysema group mice are significantly higher than in the control group(P<0.01 and P<0.05, respectively). As compared to the control group and the emphysema group, the concentration of IL-13 in the BALF of fibrosis group is significantly higher(P<0.01,both).The proportion of CD4+CD25+ regulatory T cell in the fibrosis group is significantly higher than that in the control group(P<0.03), while that in the emphysema group is significantly lower than in the control group(P<0.05). The IL-10 content in the fibrosis group is significantly lower than that in the control group(P<0.05), while in the emphysema group this index is significantly lower than in the control group(P<0.05).Conclusions: The mice pulmonary emphysema is manifested by Th1 polarization, and the mice pulmonary fibrosis is represented by Th2 polarization. CD4+CD25+ regulatory T cell facilitates the differentiation of th0 to th2, which is regulated by IL-10.
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