Effect and mechanism of imbalance via Th9 cells and Th17/Treg cells in inflammatory and fibrotic phases of pulmonary fibrosis in mice.

We investigate the role and mechanism of imbalance via Th9 cells and Th17/Treg cells in the inflammatory and fibrotic phases of pulmonary fibrosis in mice. A total of mice were split into normal saline (control group) and inflammation and fibrosis mouse models (study group) randomly, and lung tissues and bronchoalveolar lavage fluid (BALF) were obtained from mice at the inflammatory and fibrotic phases on the 7th and 28th day, respectively. The degenerative changes in the mouse lung tissue were then visible using H&E staining. The expression of CCR6 and IL-9 in the lung tissues of two groups was examined through an immunohistochemistry assay. Fluorescence PCR was used to assess the expression of PU.1 mRNA in BALF, and flow cytometry was performed to identify the expression of Th17 and Treg. (1). The level of pulmonary fibrosis and lung inflammation in the research group was significantly higher than in the control group. (2). The expression of Th17, CCR6, IL-9 and PU.1 mRNA was substantially higher (P<0.05) in the research group at different time points; the expression level of Treg cells was considerably lower (P<0.05) in the research group than in the control group. (3). CCR6, IL-9 and PU.1 mRNA levels were statistically directly associated (P<0.05) with Th17 and inversely correlated 40 with Regulatory T cells (Tregs). CCR6 and Th9 cells may be involved in 45 developing Th17/Treg imbalance in the immune inflammation of pulmonary fibrosis, which promotes fibrocyte proliferation in lung tissue.