FOXP3(+)Treg/Th17 cell imbalance in lung tissues of mice with asthma.

Immunocyte imbalances, particularly of Th1 and Th2 type helper T (Th) cells, have been implicated in the pathogenesis of chronic inflammatory diseases like asthma. Recent studies have suggested an important role for the balance between Th17 cells and FOXP3(+) regulatory T cells (Treg). However, whether this balance is important in asthma remains unknown. This study sought to detect the populations of T cell subtypes (Th1, Th2, FOXP3(+) Treg, Th17) in lung tissue of a mouse model of asthma to understand the significance of immunocyte balances in the disease. An asthma model was generated by sensitizing ten pathogen-free BALB/c mice using a standard ovalbumin challenge; ten other mice were challenged with PBS to serve as a control group. Total white cells and differential cell counts were determined in bronchoalveolar lavage fluid, and percentages of T cell subtypes were determined using flow cytometry. The severity of inflammation in lung tissue was evaluated in tissue sections, and airway hyperresponsiveness was assessed by unrestrained plethysmography. In mice with asthma, compared to those in the control group, total white cell, eosinophil, monocyte, and lymphocyte cell counts were higher, and lung inflammation and airway hyperresponsiveness were more severe (P<0.05), indicating that the model of asthma was successfully generated. Further, mice with asthma had higher percentages of Th2 and Th17 cells and lower percentages of Th1 and Foxp3(+) Treg cells in lung tissue (P<0.05). Consequently, the ratios of Th1/Th2 cells and FOXP3(+)Treg/Th17 cells were higher in the asthma group (P<0.05). Thus, in addition to the imbalance of Th1/Th2 cells, an imbalance of FOXP3(+)Treg/Th17 cells may play an important role in the pathogenesis of asthma.