IL‑33/ST2 pathway in a bleomycin‑induced pulmonary fibrosis model.

Abstract

The present study aimed to investigate the interleukin (IL)‑33/ST2 pathway in a model of acute pulmonary fibrosis, and to examine the pathogenesis of pulmonary fibrosis. The pulmonary fibrosis model was established by a single exposure to bleomycin (BLM group) endotracheally to represent idiopathic pulmonary fibrosis, and a control (Cont) group was treated with the same volume of saline. The degrees of acute injury, inflammation and fibrosis were detected using hematoxylin and eosin and Masson's staining. The IL‑33, ST2, myeloid differentiation primary response88 (MyD88) and tumor necrosis factor receptor‑associated factor6 (TRAF6) proteins were detected using Western blotting. The serum levels of IL‑4 and IL‑13 were detected using an enzyme‑linked immunosorbent assay. The results indicated that, compared with the Cont group, there were significant differences in the alveolitis scores in the BLM group on days3,7,14 and28 (P<0.01). The grades of fibrosis were also significantly different on days7, 14 and 28 (P<0.01). On examining the dynamic protein expression levels of IL‑33, ST2, MyD88 and TRAF6, the expression of IL‑33 in the BLM group increased initially, and then decreased gradually following a peak on day7. The significant differences between the BLM and Cont groups were observed on days3 and 7 (P<0.05). Compared with the Cont group, the protein levels of ST2, MyD88 and TRAF6 in the BLM group exhibited an increasing trend from day3, with significant differences, compared with the Cont group, on days3, 7, 14 and 28 (P<0.05). On examination of the serum levels of IL‑4 and IL‑13 in each group, the levels of IL‑4 and IL‑13 in BLM group remained higher from day7, with peaks on day28, and were significantly different, compared with the Cont group, on days7,14 and 28 (P<0.05). In conclusion, the IL‑33/ST2 signaling pathway was found to be involved in the rodent model of pulmonary fibrosis induced by bleomycin.