[Expression and protective effect of chemerin in idiopathic pulmonary fibrosis].

Objective: To explore the expression and the role of chemerin in idiopathic pulmonary fibrosis (IPF). Methods: Quantitative PCR and Western blotting were used to determine the mRNA and protein levels of chemerin in lung tissues from IPF patients and the controls. Clinical serum level of chemerin was analyzed by enzyme-linked immunosorbent assay. The mouse lung fibroblasts isolated and cultured in vitro were divided into the control, TGF-ß, TGF-ß+chemerin and chemerin groups. Immunofluorescence staining was used to observe the expression of α-smooth muscle actin (α-SMA). C57BL/6 mice were randomly divided into the control, bleomycin, bleomycin+chemerin, and chemerin groups. Masson and immunohistochemical staining were performed to evaluate the severity of pulmonary fibrosis. Expression of epithelial to mesenchymal transition (EMT) markers was detected by quantitative PCR and immunohistochemical staining in the in vitro and in vivo models of pulmonary fibrosis, respectively. Results: Compared with the control group, the expression of chemerin was downregulated in both the lung tissue and the serum of IPF patients. Immunofluorescence showed that treatment of fibroblasts with TGF-ß alone resulted in a robust expression of α-SMA, whereas treatment with TGF-ß and chemerin together exhibited the similar expression levels of α-SMA as the control group. Masson staining indicated that the bleomycin-induced pulmonary fibrosis model was constructed successfully, while treatment of chemerin partially alleviated the damage of lung tissue. Immunohistochemical staining showed that the expression of chemerin in the lung tissue was significantly decreased in the bleomycin group. Quantitative PCR and immunohistochemistry showed that chemerin attenuated EMT induced by TGF-ß and bleomycin both in vitro and in vivo. Conclusions: The expression of chemerin was reduced in patients with IPF. Chemerin may play a protective role in the development of IPF by regulating EMT, providing a new idea for the clinical treatment of IPF.

[Influencing factors for postoperative survival of patients with stage III silicosis treated by lung transplantation].

Objective: To investigate the clinical effect, postoperative complications, and causes of death in the treatment of stage III silicosis with lung transplantation and the influencing factors for survival. Methods: A retrospective analysis was performed for the clinical data of 32 patients with stage III silicosis who underwent lung transplantation in our hospital from September 2002 to September 2015. The survival, causes of death, and postoperative complications were analyzed. The Kaplan-Meier method was used to plot survival curves, the log-rank test was used to compare the influence of each factor on survival rates, and the multivariate Cox proportional hazards regression model was used to evaluate the influence of each factor on survival. Results: All the patients underwent successful lung transplantation. The 3-month and 1-, 3-, and 5-year postoperative cumulative survival rates were 90.6%, 80.8%, 76.7%, and 76.7%, respectively. Eight patients died during the postoperative follow-up, among whom 1 died of multiple organ failure, 3 died of severe infection, 2 died of sudden cardiac death, 1 died of renal failure, and 1 died of bronchiolitis obliterans. The major postoperative complications included primary graft dysfunction (PGD) in 10 patients, severe infection in 7 patients, acute rejection reaction in 3 patients, bronchiolitis obliterans in 5 patients, bleeding in 5 patients, anastomotic complication in 2 patients, and renal dysfunction in 3 patients. The Kaplan-Meier survival analysis showed that sex, postoperative PGD, postoperative infection, massive intraoperative blood loss, preoperative pulmonary arterial hypertension were influencing factors for postoperative survival rates (P<0.05). The multivariate Cox regression model showed that male sex was the protective factor (P<0.05) and postoperative PGD and massive intraoperative blood loss were independent risk factors for death after transplantation (P<0.05). Conclusion: Lung transplantation is a method for the treatment of silicosis. Postoperative PGD and massive intraoperative blood loss are independent risk factors for death after transplantation. Survival rates are affected by postoperative PGD, infection, massive intraoperative blood loss, and preoperative pulmonary arterial hypertension.