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Dongru Du,1– 3,* Bi Ran,1– 3,* Dan Xu,1– 3 Lian Liu,1– 3 Xueru Hu,1– 3 Tingting Zeng,1– 3 Yongchun Shen,1– 3 Fengming Luo1– 4 1Department of Pulmonary and Critical Care Medicine, West China Hospital, Sichuan University, Chengdu, 610041, People’s Republic of China; 2State Key Laboratory of Respiratory Health and Multimorbidity, West China Hospital, Sichuan University, Chengdu, 610041, People’s Republic of China; 3Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital, Sichuan University, Chengdu, 610041, People’s Republic of China; 4Laboratory of Pulmonary Immunology and Inflammation, Frontiers Science Center for Disease-Related Molecular Network, Sichuan University, Chengdu, 610200, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yongchun Shen; Fengming Luo, Tel +86 28 8542 2350, Fax +86 28 8558 2944, Email shen_yongchun@126.com; fengmingluo@outlook.comBackground: Sex steroid hormones, including testosterone and estradiol, play significant roles in various aspects of pulmonary health and diseases. However, although there were a few studies trying to link sex hormones with COPD, their effect remained limited due to small sample size and insufficient causal results. This study aims to investigate the association between sex hormones and chronic obstructive pulmonary disease (COPD) based on the National Health and Nutrition Examination Survey (NHANES) database and evaluate causality via a two-sample Mendelian randomization (MR).Methods: Data from NHANES 2013– 2016 were enrolled for the cross-sectional study. The association between sex hormones and COPD was evaluated via multivariable logistic regression. Sex-stratified analysis, subgroup analyses and interaction tests were performed to further evaluate the correlation. For MR analysis, data were collected from genome-wide association studies and FinnGen datasets. The inverse-variance-wei

Junjie Peng,* Min Wang,* Yanqiu Wu,* Yongchun Shen, Lei Chen Department of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, People’s Republic of China*These authors contributed equally to this workCorrespondence: Lei Chen; Yongchun Shen, Department of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, People’s Republic of China, Email lchens@126.com; shen_yongchun@126.comBackground: Some clinical indicators have been reported to be useful in differentiating asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) from pure asthma/COPD, but the results were inconsistent. This study aims to evaluate the diagnostic value of these indicators for ACO.Methods: Databases of PubMed, EMBASE, Ovid and Web of Science were retrieved. Pooled standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated in random-effects models.Results: 48 eligible studies were included. The pooled results indicated, compared with pure asthma, ACO patients had lower levels of forced expiratory volume in the first second (FEV1)% predicted (pred) (SMD=− 1.09, 95% CI − 1.3 to − 0.87), diffusion lung capacity for carbon monoxide (DLCO)% pred (SMD=− 0.83, 95% CI − 1.24 to − 0.42), fractional exhaled nitric oxide (FeNO) (SMD=− 0.23, 95% CI − 0.36 to − 0.11), and higher levels of induced sputum neutrophil (SMD = 0.51, 95% CI 0.21 to 0.81), circulating YKL-40 (SMD = 0.96, 95% CI 0.27 to 1.64). However, relative to COPD alone, ACO patients had higher levels of FEV1% pred (SMD = 0.15, 95% CI 0.05 to 0.26), DLCO% pred (SMD = 0.38, 95% CI 0.16 to 0.6), FeNO (SMD = 0.59, 95% CI 0.40 to 0.78), serum total immunoglobulin (Ig)E (SMD = 0.42, 95% CI 0.1 to 0.75), blood eosinophil (SMD = 0.44, 95% CI 0.29 to 0.59), induced sputum eosinophil (SMD = 0.62, 95% CI 0.42 to 0.83), and lower le

Ping Li,1,* Junjie Peng,1,* Guangxi Chen,1,2,* Fangying Chen,1,3 Yongchun Shen,1 Lin Liu,4 Lei Chen1 1Laboratory of Pulmonary Diseases and Department of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, People’s Republic of China; 2Department of Sleep Medicine, Jiujiang First People’s Hospital, Jiujiang, People’s Republic of China; 3Department of Tuberculosis, the Third People’s Hospital of Tibet Autonomous Region, Lhasa, People’s Republic of China; 4Department of Respiratory and Critical Care Medicine, 363 Hospital, Chengdu, People’s Republic of China*These authors contributed equally to this workCorrespondence: Lei Chen, Department of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, People’s Republic of China, Email lchens@126.com Lin Liu, Department of Respiratory and Critical Care Medicine, 363 Hospital, Chengdu, People’s Republic of China, Email lliniu@126.comPurpose: DNA methylation, a major epigenetic modification, has been documented to play an important role in chronic obstructive pulmonary disease (COPD). In this study, we aimed to profile the DNA methylation patterns in a mouse model of airway inflammation induced by cigarette smoke (CS), a foremost risk factor of COPD.Material and Methods: To establish a model of airway inflammation, wild-type mice were exposed to mainstream CS or room air for 2 hours twice daily, 6 days per week for consecutive 4 weeks. Lung tissues of the mice were collected for genome-wide DNA methylation analysis by liquid hybridization capture-based bisulfite sequencing, which were used for intersection analysis with gene expression by cDNA microarray to identify candidate methylated genes. Then, functional enrichment analyses with protein–protein interaction (PPI) network regarding these genes were conducted to explore the potential mechanism

Jing An, Ting Yang, Jiajia Dong, Zenglin Liao, Chun Wan, Yongchun Shen, Lei Chen Department of Respiratory and Critical Care Medicine, Division of Pulmonary Diseases, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, People’s Republic of ChinaCorrespondence: Yongchun Shen; Lei Chen Email shen_yongchun@126.com; lchens@126.comBackground: Chronic obstructive pulmonary disease (COPD) is a heterogeneous chronic inflammatory disease characterized by progressive airflow limitation that causes high morbidity and mortality. MicroRNA, a short-chain noncoding RNA, regulates gene expression at the transcriptional level. microRNA modules with a role in the pathogenesis of COPD may serve as COPD biomarkers.Methods: We downloaded the GSE33336 microarray data set from the Gene Expression Omnibus (GEO) database, the data are derived from 29 lung samples of patients with emphysema undergoing curative resection for lung cancer. We used weighted gene co-expression network analysis (WGCNA) to construct co-expression modules and detect trait-related microRNA modules. We used the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis to predict the biological function of the interest modules, and we screened out candidate hub microRNAs based on their module membership (MM) value and top proteins on the results of the protein–protein interaction (PPI) network.Results: Three microRNA modules (royal blue, light yellow and grey60) were highly associated with COPD. Axon guidance, proteoglycans in cancer and mitogen-activated protein kinases (MAPK) signaling pathway were common pathways in these three modules. Keratin18 (KRT18) was the top protein in our study. miR-452, miR-149, miR-133a, miR-181a and miR-421 in hub microRNAs may play a role in COPD.Conclusion: These findings provide evidence for the role of miRNAs in COPD and identify biomarker candidates.Keywords: chronic obstructive pulmonary disease, weight

Mei Yang,&ast; Ting Yang,&ast; Xiaoou Li,&ast; Diandian Li, Zenglin Liao, Yongchun Shen, Dan Xu, Lei Chen, Fuqiang Wen Department of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, Sichuan, 610041, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Lei Chen; Fuqiang WenDepartment of Respiratory and Critical Care Medicine, West China Hospital, West China School of Medicine, Sichuan University, Chengdu, Sichuan, 610041, People’s Republic of ChinaEmail lchens@126.com; wenfuqiang@scu.edu.cnPurpose: Elevated blood eosinophils have been implicated in chronic obstructive pulmonary disease (COPD) progression and exacerbation. We aim to investigate clinical predictors of high blood eosinophils in a Chinese COPD cohort.Patients and Methods: We conducted a retrospective cohort study in Sichuan province, a Southwest province with high prevalence of COPD in China. All patients in this cohort were extracted from the Chinese Pulmonary Health study, a large cross-sectional study on COPD epidemiology in China. Demographics, personal and family history, living condition, spirometry and blood eosinophil counts were obtained. Univariate and multiple linear regression analyses were performed to determine predictors of high blood eosinophils.Results: A total of 375 COPD patients were included in this cohort. The median absolute blood eosinophil count was 138.8 cells/μL, and the prevalence of COPD with high blood eosinophils was 66.7% and 14.7% when using the thresholds of 100 cells/μL and 300 cells/μL, respectively. Univariate analyses indicated that male gender, lower body mass index, high-density lipoprotein (HDL), lower family income, raising pets and biomass use were significantly associated with high blood eosinophils (p < 0.05). Multiple linear regression model further revealed male gender (unstandardized coefficient (B)=66.125, 95% confidence

Yanqiu Wu,1,2 Jiangyue Qin,1,2 Junyun He,3 Yongchun Shen,1,2 Hao Wang,1,2 Yanping Li,4 Qianglin Zeng,5 Jiajia Dong,1,2 Yunfei An,6 Shuguang Xiong,7 Mei Feng,2 Fuqiang Wen1,2 1Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People’s Republic of China; 2Department of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People’s Republic of China; 3Department of Respiratory and Critical Care Medicine, Hospital of Chengdu Office of People’s Government of Tibetan Autonomous Region, Chengdu, Sichuan, People’s Republic of China; 4Department of Respiratory and Critical Care Medicine, Third People’s Hospital of Chengdu, Sichuan, People’s Republic of China; 5Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Chengdu University, Chengdu, Sichuan, People’s Republic of China; 6Department of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People’s Republic of China; 7Department of Respiratory and Critical Care Medicine, 416 Hospital of Nuclear Industry, Chengdu, Sichuan, People’s Republic of ChinaCorrespondence: Fuqiang WenDivision of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu 610041, Sichuan, People’s Republic of ChinaTel +86-28-8542 2350Email wenfuqiang@scu.edu.cnBackgrounds and Aims: It is well known that angiogenesis contributes to the progression of chronic obstructive pulmonary disease (COPD) by initiating the remodeling of bronchial vasculature. However, the specific molecular mechanisms are incompletely understood. This research aimed to explore whether endostatin, a member of endogenous antiangiogenic proteins, is a biomarker in COPD and plays a role in the angiogenesis of COPD.Methods: 100 stable COPD pati