L Y Zhang1, J Chen1, Y Zhang2, Y H Gu1, X M Rao1, Y Ouyang1. 1. The First Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, China. 2. Department of Internal Medicine, Affiliated Hospital of Maternal and Child Health Care of Zunyi Medical University, Zunyi, Guizhou 563000, China.
Abstract
Objective: To explore the role of lung dendritic cells (DCs) and Th17/regulatory T cells (Treg) pathway in the pathogenesis of chronic obstructive pulmonary disease(COPD). Methods: COPD patients who received lobectomy from Sep. 2015 to Mar. 2016 in our hospital were enrolled and classified into non-smoking non-COPD group, smoking without COPD group and COPD group. The expression of CD(80), chemokine recepter-6 (CCR6), interleukin-17A (IL-17A) and fork-head transcription factor P3 (FoxP3) were detected by immunohistochemistry (IHC) in lung tissue. Mature DCs (mDCs), immature DCs (imDCs), Th17 cells and Treg cells in lung tissue were detected by flow cytometry (FCM) and the correlation between Th17/Treg cells with lung function was analyzed. Results: (1) The expression of CD(80) and FoxP3 in COPD group was decreased, while the expression of CCR6 and IL-17A was increased (P<0.05). (2) The percentage of mDCs and Treg in lung tissue of COPD group was significantly decreased. In contrast, the proportion of imDCs and Th17 cells in COPD group was significantly increased (P<0.05). (3) The imbalance of Th17/Treg ratio in lung tissue was seen in patients with COPD, suggesting the potential mechanism of Th17 cell-mediated proinflammatory response. (4) The percentage of Th17 cells and Th17/Treg ratio in COPD patients was negatively correlated with forced expiratory volume in the first second (FEV(1)) as a percentage of predicted value (FEV(1)% pred), forced vital capacity(FVC) as a percentage of predicted value (FVC% pred), FEV(1)/FVC. On the other hand, the percentage of Treg cells was positively correlated with FEV(1)% pred, FVC% pred, FEV(1)/FVC. Conclusions: The data in this study demonstrate the maturation disorder of dendritic cells in lung tissue of COPD patients. The imbalance of Th17/Treg ratio suggests that Th17 cell-mediated proinflammatory response may be involved in the pathogenesis of COPD.
Objective: To explore the role of lung dendritic cells (DCs) and Th17/regulatory T cells (Treg) pathway in the pathogenesis of chronic obstructive pulmonary disease(COPD). Methods: COPD patients who received lobectomy from Sep. 2015 to Mar. 2016 in our hospital were enrolled and classified into non-smoking non-COPD group, smoking without COPD group and COPD group. The expression of CD(80), chemokine recepter-6 (CCR6), interleukin-17A (IL-17A) and fork-head transcription factor P3 (FoxP3) were detected by immunohistochemistry (IHC) in lung tissue. Mature DCs (mDCs), immature DCs (imDCs), Th17 cells and Treg cells in lung tissue were detected by flow cytometry (FCM) and the correlation between Th17/Treg cells with lung function was analyzed. Results: (1) The expression of CD(80) and FoxP3 in COPD group was decreased, while the expression of CCR6 and IL-17A was increased (P<0.05). (2) The percentage of mDCs and Treg in lung tissue of COPD group was significantly decreased. In contrast, the proportion of imDCs and Th17 cells in COPD group was significantly increased (P<0.05). (3) The imbalance of Th17/Treg ratio in lung tissue was seen in patients with COPD, suggesting the potential mechanism of Th17 cell-mediated proinflammatory response. (4) The percentage of Th17 cells and Th17/Treg ratio in COPD patients was negatively correlated with forced expiratory volume in the first second (FEV(1)) as a percentage of predicted value (FEV(1)% pred), forced vital capacity(FVC) as a percentage of predicted value (FVC% pred), FEV(1)/FVC. On the other hand, the percentage of Treg cells was positively correlated with FEV(1)% pred, FVC% pred, FEV(1)/FVC. Conclusions: The data in this study demonstrate the maturation disorder of dendritic cells in lung tissue of COPD patients. The imbalance of Th17/Treg ratio suggests that Th17 cell-mediated proinflammatory response may be involved in the pathogenesis of COPD.