Additional file 1: of Long-term smoking alters abundance of over half of the proteome in bronchoalveolar lavage cell in smokers with normal spirometry, with effects on molecular pathways associated with COPD

Table S1. Clinical characteristics of subjects, stratified by gender. Table S2. Proteins significantly altered between Smoker vs Never-smoker groups. Table S3. Proteins significantly altered between female Smoker vs Never-smoker groups. Table S4. Proteins significantly altered between male Smoker vs Never-smoker groups. Table S5. Significantly enriched pathways and associated proteins when comparing Smoker and Never-smoker groups. Table S6. Significantly enriched pathways following stratification by gender when comparing Smoker and Never-smoker groups. (XLSX 1321 kb

Additional file 2: of Long-term smoking alters abundance of over half of the proteome in bronchoalveolar lavage cell in smokers with normal spirometry, with effects on molecular pathways associated with COPD

Figure S1. The OPLS-DA modeling parameters for joint gender, female and male Smoker vs. Never-smoker. Permutation test was performed 200 times for each model. Figure S2. Leukocyte transendothelial migration was significantly altered in joint smokers. ITGAM, P11215, Integrin alpha-M (CD11b); ITGB2, P05107, Integrin beta-2 (CD18); PECAM1, P16284, Platelet endothelial cell adhesion molecule; JAM-A, Q9Y624, Junctional adhesion molecule A; MLC-2, O14950, Myosin regulatory light chain 12B; CDC42, P60953, Cell division control protein 42 homolog; Actin, P60709, actin cytoplasmic 1; α-actin, P12814, O43707, α-actinin-1, α-actinin-4, respectively; NOX2, P04839, Cytochrome b-245 heavy chain; p40phox, Q15080, Neutrophil cytosol factor 4; RAC2, P15153, Ras-related C3 botulinum toxin substrate 2; RAP1A, P62834, Ras-related protein Rap-1A. (DOC 1606 kb

Additional file 1: of Proteomic profiling of lung immune cells reveals dysregulation of phagocytotic pathways in female-dominated molecular COPD phenotype

Supplementary Methods. Figure S1. Analysis of Share and Unique Structure (SUS) between OPLS-DA models of female Smoker vs COPD (x-axis) and Never-smoker vs ex-smoker with COPD (exCOPD) (y-axis). Figure S2. Multivariate sensitivity analysis of the impact of menopausal status on proteomic profiling in female COPD patients. Figure S3. The percentage of CT attenuation values <−950 HU in the Smoker and COPD groups, stratified by gender. (DOC 1849 kb

Additional file 2: of Proteomic profiling of lung immune cells reveals dysregulation of phagocytotic pathways in female-dominated molecular COPD phenotype

Table S1. Heterogeneity indeces (I2) for proteins significantly altered between Smoker vs COPD groups joint gender as well as gender stratified models. Table S2. Protein identities and model statistics of proteins of interest from OPLS-DA models comparing Smoker and COPD groups for joint gender as well as gender stratified models. Table S3. Uniprot accessions, gene names, protein names, as well as and direction of alteration for proteins involved in pathways significantly altered due to COPD. Table S4. Pathways significantly enriched in female vs male COPD patients. Table S5. Names and MS/MS data of proteins used in statistical analyses. Table S6. Significantly altered proteins i Smoker vs COPD groups, stratified by gender. (XLSX 338 kb