Abstract: AIM : To investigate the changes of Treg and related cytokines in cigarette smoke-induced mice model of chronic airway inflammation, and to explore the role of Treg in the pathogenesis of COPD.METHODS: Sixty male BALB/c mice were randomly divided into 3 groups: a 24 wk smoke chronic exposure group, a 4 wk sub-acute exposure group and control group(n=20 each). Cells in BALF were collected and analyzed by absolute and differential cell counts. IL-6, TGF-β and IL-10 levels in serum and BALF were tested by enzyme linked immunosorbent assay (ELISA). The proportion of CD₄^＋Foxp3^＋Treg in peripheral blood mononuclear cell (PBMC) and lung tissue were determined by flow cytometry. The mRNA expressions of Foxp3 in lung tissues were measured by real-time PCR.RESULTS:Ratio of Treg was higher in the sub-acute smoke-exposure group in lung tissue(5.24％±0.86%)and peripheral blood (5.24％±1.23%) compared with the control group[(2.52±0.62)%, (3.54±0.87)%]. But the ratio of Treg in the chronic exposure group in lung tissue (1.83％±0.39％) and peripheral blood (1.88％±0.25％)was lower compared with the control group, all P<0.01. The level of Foxp3 mRNA in lung tissue was increased in the sub-acute smoke-exposure (2.67±0.73) compared with the control groups (1.49±0.37).But it was remarkably decreased in the chronic exposure group (0.61±0.21) compared with the control groups, P<0.01. Levels of IL-6 and TGF-β were remarkably increased in the chronic exposure group in serum[(56.47±19.41) pg/mL, (144.22±43.19 pg/mL)] compared with the sub-acute smoke-exposure group[(6.22±2.06 pg/mL), (23.32±8.32 pg/mL)] and the control group[(5.12±1.48 pg/mL), (18.14±13.00 pg/mL)], all P<0.01. IL-10 in serum was significantly decreased in the chronic smoke-exposure group (4.04±2.57 pg/mL) compared with the control group(8.26±2.02 pg/mL), and it was increased in sub-acute smoke-exposure group (10.42±2.45 pg/mL) compared with the control group, all P<0.01.CONCLUSION: Our study thus reveals that the change of Treg and the related cytokines exists in mice with sub-acute and chronic cigarette smoke exposure, suggesting its potential role in the breakdown of immune self-tolerance in chronic airway inflammatory response. Further research on Treg change in airway inflammation of COPD may provide insights into the development of new therapeutic targets for this disease.

Key words: regulatory T cells, cigarette exposure, airway inflammation, chronic obstructive pulmonary disease, model, animals