The mechanisms and significance of IL-33/ST2 in COPD

In order to investigate the mechanisms and significance of IL-33/ST2 in COPD, we recruited 90 subjects undergoing lung resection for solitary peripheral carcinoma in our hospital who were divided into three groups equally and randomly: non-smokers, smokers with normal lung function and COPD patients according to their clinical characteristics. When compared with the non-smokers, smokers with normal lung function, the majority of the COPD patients have a hobby of smoking and a weak lung function. The expression of IL-33, IL-1RAcP, ST2, IL-13, MUC5AC, Chi3l3, IL-25, TSLP, SCGB3A1, SFTPC, Krt5, Aq3, Trp63 and Ngfr were dramatically increased in the hTECs of COPD patients and all the genes were highly correlated with the IL-33/ST2 signal. When the IL-33/ST2 signal was interrupted, the expression pattern of these genes were reversed; the phosphorylation level of MEKKK, p38MAPK11, NIK1, I kappa B, TAK1, NF-kappa B, JNK1, 2, 3 and ERK1/2 were obviously elevated in the hTECs of COPD patients, all of which were involved in the pathogenesis of COPD but the exact correlation with IL-33/ST2 remains further investigation. These results demonstrated that the activity of IL-33/ST2 was enhanced dramatically in COPD patients, the canonical NF-kappa B signal pathway was activated when the IL-33/ST2 was enhanced in COPD, and the inflammatory cytokines associated with Th2 responses were secreted abundantly leading to pneumonia and bronchitis. So we propose that IL-33/ST2 is the gold standard diagnosis indicator of COPD and will provide the well-known knowledge for the clinical diagnosis and treatment.