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Your search keyword '"Pavlidis, Stelios"' showing total 6 results
Start Over Author "Pavlidis, Stelios" Publisher karolinska inst, stockholm, sweden
6 results on '"Pavlidis, Stelios"'

1. Blood eosinophil count and airway epithelial transcriptome relationships in COPD versus asthma

Author

George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, Brightling, Christopher E., George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, and Brightling, Christopher E.

Abstract

Background: Whether the clinical or pathophysiologic significance of the "treatable trait" high blood eosinophil count in COPD is the same as for asthma remains controversial. We sought to determine the relationship between the blood eosinophil count, clinical characteristics and gene expression from bronchial brushings in COPD and asthma. Methods: Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED). We determined gene expression using RNAseq in EvA (n = 283) and Affymetrix microarrays in U-BIOPRED (n = 85). We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood eosinophil counts as well as differential expression using a blood eosinophil > 200 cells/mu L as a cut-off. The false discovery rate was controlled at 1% (with continuous values) and 5% (with dichotomized values). Results: There were no differences in age, gender, lung function, exercise capacity and quantitative computed tomography between eosinophilic versus noneosinophilic COPD cases. Total serum IgE was increased in eosinophilic asthma and COPD. In EvA, there were 12 genes with a statistically significant positive association with the linear blood eosinophil count, whereas in U-BIOPRED, 1197 genes showed significant associations (266 positive and 931 negative). The transcriptome showed little overlap between genes and pathways associated with blood eosinophil counts in asthma versus COPD. Only CST1 was common to eosinophilic asthma and COPD and was replicated in independent cohorts. Conclusion: Despite shared "treatable traits" between asthma and COPD, the molecular mechanisms underlying these clinical entities are predominately different.

Published
2020
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2. Blood eosinophil count and airway epithelial transcriptome relationships in COPD versus asthma

Author

George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, Brightling, Christopher E., George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, and Brightling, Christopher E.

Abstract

Background: Whether the clinical or pathophysiologic significance of the "treatable trait" high blood eosinophil count in COPD is the same as for asthma remains controversial. We sought to determine the relationship between the blood eosinophil count, clinical characteristics and gene expression from bronchial brushings in COPD and asthma. Methods: Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED). We determined gene expression using RNAseq in EvA (n = 283) and Affymetrix microarrays in U-BIOPRED (n = 85). We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood eosinophil counts as well as differential expression using a blood eosinophil > 200 cells/mu L as a cut-off. The false discovery rate was controlled at 1% (with continuous values) and 5% (with dichotomized values). Results: There were no differences in age, gender, lung function, exercise capacity and quantitative computed tomography between eosinophilic versus noneosinophilic COPD cases. Total serum IgE was increased in eosinophilic asthma and COPD. In EvA, there were 12 genes with a statistically significant positive association with the linear blood eosinophil count, whereas in U-BIOPRED, 1197 genes showed significant associations (266 positive and 931 negative). The transcriptome showed little overlap between genes and pathways associated with blood eosinophil counts in asthma versus COPD. Only CST1 was common to eosinophilic asthma and COPD and was replicated in independent cohorts. Conclusion: Despite shared "treatable traits" between asthma and COPD, the molecular mechanisms underlying these clinical entities are predominately different.

Published
2020
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3. Blood eosinophil count and airway epithelial transcriptome relationships in COPD versus asthma

Author

George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, Brightling, Christopher E., George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, and Brightling, Christopher E.

Abstract

Background: Whether the clinical or pathophysiologic significance of the "treatable trait" high blood eosinophil count in COPD is the same as for asthma remains controversial. We sought to determine the relationship between the blood eosinophil count, clinical characteristics and gene expression from bronchial brushings in COPD and asthma. Methods: Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED). We determined gene expression using RNAseq in EvA (n = 283) and Affymetrix microarrays in U-BIOPRED (n = 85). We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood eosinophil counts as well as differential expression using a blood eosinophil > 200 cells/mu L as a cut-off. The false discovery rate was controlled at 1% (with continuous values) and 5% (with dichotomized values). Results: There were no differences in age, gender, lung function, exercise capacity and quantitative computed tomography between eosinophilic versus noneosinophilic COPD cases. Total serum IgE was increased in eosinophilic asthma and COPD. In EvA, there were 12 genes with a statistically significant positive association with the linear blood eosinophil count, whereas in U-BIOPRED, 1197 genes showed significant associations (266 positive and 931 negative). The transcriptome showed little overlap between genes and pathways associated with blood eosinophil counts in asthma versus COPD. Only CST1 was common to eosinophilic asthma and COPD and was replicated in independent cohorts. Conclusion: Despite shared "treatable traits" between asthma and COPD, the molecular mechanisms underlying these clinical entities are predominately different.

Published
2020
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4. Blood eosinophil count and airway epithelial transcriptome relationships in COPD versus asthma

Author

George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, Brightling, Christopher E., George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, and Brightling, Christopher E.

Abstract

Background: Whether the clinical or pathophysiologic significance of the "treatable trait" high blood eosinophil count in COPD is the same as for asthma remains controversial. We sought to determine the relationship between the blood eosinophil count, clinical characteristics and gene expression from bronchial brushings in COPD and asthma. Methods: Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED). We determined gene expression using RNAseq in EvA (n = 283) and Affymetrix microarrays in U-BIOPRED (n = 85). We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood eosinophil counts as well as differential expression using a blood eosinophil > 200 cells/mu L as a cut-off. The false discovery rate was controlled at 1% (with continuous values) and 5% (with dichotomized values). Results: There were no differences in age, gender, lung function, exercise capacity and quantitative computed tomography between eosinophilic versus noneosinophilic COPD cases. Total serum IgE was increased in eosinophilic asthma and COPD. In EvA, there were 12 genes with a statistically significant positive association with the linear blood eosinophil count, whereas in U-BIOPRED, 1197 genes showed significant associations (266 positive and 931 negative). The transcriptome showed little overlap between genes and pathways associated with blood eosinophil counts in asthma versus COPD. Only CST1 was common to eosinophilic asthma and COPD and was replicated in independent cohorts. Conclusion: Despite shared "treatable traits" between asthma and COPD, the molecular mechanisms underlying these clinical entities are predominately different.

Published
2020
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5. Blood eosinophil count and airway epithelial transcriptome relationships in COPD versus asthma

Author

George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, Brightling, Christopher E., George, Leena, Taylor, Adam R., Esteve-Codina, Anna, Soler Artigas, Maria, Andri Thun, Gian, Bates, Stewart, Pavlidis, Stelios, Wagers, Scott, Boland, Anne, Prasse, Antje, Boschetto, Piera, Parr, David G., Nowinski, Adam, Barta, Imre, Hohlfeld, Jens, Greulich, Timm, van den Berge, Maarten, Hiemstra, Pieter S., Timens, Wim, Hinks, Timothy, Wenzel, Sally, Siddiqui, Salman, Richardson, Matthew, Venge, Per, Heath, Simon, Gut, Ivo, Tobin, Martin D., Edwards, Lindsay, Riley, John H., Djukanovic, Ratko, Auffray, Charles, De-Meulder, Bertrand, Erik-Dahlen, Sven, Adcock, Ian M., Chung, Kian Fan, Ziegler-Heitbrock, Loems, Sterk, Peter J., Singh, Dave, and Brightling, Christopher E.

Abstract

Background: Whether the clinical or pathophysiologic significance of the "treatable trait" high blood eosinophil count in COPD is the same as for asthma remains controversial. We sought to determine the relationship between the blood eosinophil count, clinical characteristics and gene expression from bronchial brushings in COPD and asthma. Methods: Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma cohort (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes, U-BIOPRED). We determined gene expression using RNAseq in EvA (n = 283) and Affymetrix microarrays in U-BIOPRED (n = 85). We ran linear regression analysis of the bronchial brushings transcriptional signal versus blood eosinophil counts as well as differential expression using a blood eosinophil > 200 cells/mu L as a cut-off. The false discovery rate was controlled at 1% (with continuous values) and 5% (with dichotomized values). Results: There were no differences in age, gender, lung function, exercise capacity and quantitative computed tomography between eosinophilic versus noneosinophilic COPD cases. Total serum IgE was increased in eosinophilic asthma and COPD. In EvA, there were 12 genes with a statistically significant positive association with the linear blood eosinophil count, whereas in U-BIOPRED, 1197 genes showed significant associations (266 positive and 931 negative). The transcriptome showed little overlap between genes and pathways associated with blood eosinophil counts in asthma versus COPD. Only CST1 was common to eosinophilic asthma and COPD and was replicated in independent cohorts. Conclusion: Despite shared "treatable traits" between asthma and COPD, the molecular mechanisms underlying these clinical entities are predominately different.

Published
2020
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6. Stratification of asthma phenotypes by airway proteomic signatures

Author

Schofield, James P. R., Burg, Dominic, Nicholas, Ben, Strazzeri, Fabio, Brandsma, Joost, Staykova, Doroteya, Folisi, Caterina, Bansal, Aruna T., Xian, Yang, Guo, Yike, Rowe, Anthony, Corfield, Julie, Wilson, Susan, Ward, Jonathan, Lutter, Rene, Shaw, Dominick E., Bakke, Per S., Caruso, Massimo, Dahlen, Sven-Erik, Fowler, Stephen J., Horvath, Ildiko, Howarth, Peter, Krug, Norbert, Montuschi, Paolo, Sanak, Marek, Sandstrom, Thomas, Sun, Kai, Pandis, Ioannis, Riley, John, Auffray, Charles, De Meulder, Bertrand, Lefaudeux, Diane, Sousa, Ana R., Adcock, Ian M., Chung, Kian Fan, Sterk, Peter J., Skipp, Paul J., Djukanovic, Ratko, Ahmed, H., Allen, D., Badorrek, P., Ballereau, S., Baribaud, F., Batuwitage, M. K., Bedding, A., Behndig, A. F., Berglind, A., Berton, A., Bigler, J., Boedigheimer, M. J., Bonnelykke, K., Brinkman, P., Bush, A., Campagna, D., Casaulta, C., Chaiboonchoe, A., Davison, T., De Meulder, B., Delin, I., Dennison, P., Dodson, P., El Hadjam, L., Erzen, D., Faulenbach, C., Fichtner, K., Fitch, N., Formaggio, E., Gahlemann, M., Galffy, G., Garissi, D., Garret, T., Gent, J., Guillmant-Farry, E., Henriksson, E., Hoda, U., Hohlfeld, J. M., Hu, X., James, A., Johnson, K., Jullian, N., Kerry, G., Klueglich, M., Knowles, R., Konradsen, J. R., Kretsos, K., Krueger, L., Lantz, A. -S, Larminie, C., Latzin, P., Lefaudeux, D., Lemonnier, N., Lowe, L. A., Lutter, R., Manta, A., Mazein, A., McEvoy, L., Menzies-Gow, A., Mores, N., Murray, C. S., Nething, K., Nihlen, U., Niven, R., Nordlund, B., Nsubuga, S., Pellet, J., Pison, C., Pratico, G., Puig Valls, M., Riemann, K., Rocha, J. P., Rossios, C., Santini, G., Saqi, M., Scott, S., Sehgal, N., Selby, A., Soderman, P., Sogbesan, A., Spycher, F., Stephan, S., Stokholm, J., Sunther, M., Szentkereszty, M., Tamasi, L., Tariq, K., Valente, S., van Aalderen, W. M., van Drunen, C. M., Van Eyll, J., Vyas, A., Yu, W., Zetterquist, W., Zolkipli, Z., Zwinderman, A. H., Adriaens, Nora, Aliprantis, Antonios, Alving, Kjell, Bakke, Per, Balgoma, David, Barber, Clair, Baribaud, Frederic, Bates, Stewart, Bautmans, An, Beleta, Jorge, Bochenek, Grazyna, Braun, Armin, Carayannopoulos, Leon, Rocha, Joao Pedro Carvalho da Purificacao, Chaleckis, Romanas, D'Amico, Arnaldo, De Alba, Jorge, De Lepeleire, Inge, Dekker, Tamara, Dijkhuis, Annemiek, Draper, Aleksandra, Edwards, Jessica, Emma, Rosalia, Ericsson, Magnus, Flood, Breda, Gallart, Hector, Gomez, Cristina, Gove, Kerry, Gozzard, Neil, Haughney, John, Hewitt, Lorraine, Hohlfeld, Jens, Holweg, Cecile, Hu, Richard, Hu, Sile, Kamphuis, Juliette, Kennington, Erika J., Kerry, Dyson, Knobel, Hugo, Kolmert, Johan, Kots, Maxim, Kuo, Scott, Kupczyk, Maciej, Lambrecht, Bart, Lone-Latif, Saeeda, Loza, Matthew J., Marouzet, Lisa, Martin, Jane, Masefield, Sarah, Mathon, Caroline, Meah, Sally, Meiser, Andrea, Metcalf, Leanne, Mikus, Maria, Miralpeix, Montse, Monk, Philip, Naz, Shama, Nilsson, Peter, Ostling, Jorgen, Pacino, Antonio, Palkonen, Susanna, Pavlidis, Stelios, Pennazza, Giorgio, Petren, Anne, Pink, Sandy, Postle, Anthony, Powell, Pippa, Rahman-Amin, Malayka, Rao, Navin, Ravanetti, Lara, Ray, Emma, Reinke, Stacey, Reynolds, Leanne, Robberechts, Martine, Roberts, Amanda, Russell, Kirsty, Rutgers, Michael, Santoninco, Marco, Schoelch, Corinna, Sjodin, Marcus, Smids, Barbara, Smith, Caroline, Smith, Jessica, Smith, Katherine M., Thorngren, John-Olof, Thornton, Bob, Thorsen, Jonathan, van de Pol, Marianne, van Geest, Marleen, Versnel, Jenny, Vink, Anton, Wald, Frans, Walker, Samantha, Weiszhart, Zsoka, Wetzel, Kristiane, Wheelock, Craig E., Wiegman, Coen, Williams, Sian, Wilson, Susan J., Woodcock, Ashley, Yang, Xian, Yeyasingham, Elizabeth, Prins, Jan-Bas, Gahlemann, Martina, Visintin, Luigi, Evans, Hazel, Puhl, Martine, Buzermaniene, Lina, Hudson, Val, Bond, Laura, de Boer, Pim, Widdershoven, Guy, Sigmund, Ralf, Supple, David, Hamerlijnck, Dominique, Negus, Jenny, Kamphuis, Julitte, Sergison, Lehanne, Onstein, Susanne, MacNee, William, Bernardini, Renato, Bont, Louis, Wecksell, Per-Ake, Schofield, James P. R., Burg, Dominic, Nicholas, Ben, Strazzeri, Fabio, Brandsma, Joost, Staykova, Doroteya, Folisi, Caterina, Bansal, Aruna T., Xian, Yang, Guo, Yike, Rowe, Anthony, Corfield, Julie, Wilson, Susan, Ward, Jonathan, Lutter, Rene, Shaw, Dominick E., Bakke, Per S., Caruso, Massimo, Dahlen, Sven-Erik, Fowler, Stephen J., Horvath, Ildiko, Howarth, Peter, Krug, Norbert, Montuschi, Paolo, Sanak, Marek, Sandstrom, Thomas, Sun, Kai, Pandis, Ioannis, Riley, John, Auffray, Charles, De Meulder, Bertrand, Lefaudeux, Diane, Sousa, Ana R., Adcock, Ian M., Chung, Kian Fan, Sterk, Peter J., Skipp, Paul J., Djukanovic, Ratko, Ahmed, H., Allen, D., Badorrek, P., Ballereau, S., Baribaud, F., Batuwitage, M. K., Bedding, A., Behndig, A. F., Berglind, A., Berton, A., Bigler, J., Boedigheimer, M. J., Bonnelykke, K., Brinkman, P., Bush, A., Campagna, D., Casaulta, C., Chaiboonchoe, A., Davison, T., De Meulder, B., Delin, I., Dennison, P., Dodson, P., El Hadjam, L., Erzen, D., Faulenbach, C., Fichtner, K., Fitch, N., Formaggio, E., Gahlemann, M., Galffy, G., Garissi, D., Garret, T., Gent, J., Guillmant-Farry, E., Henriksson, E., Hoda, U., Hohlfeld, J. M., Hu, X., James, A., Johnson, K., Jullian, N., Kerry, G., Klueglich, M., Knowles, R., Konradsen, J. R., Kretsos, K., Krueger, L., Lantz, A. -S, Larminie, C., Latzin, P., Lefaudeux, D., Lemonnier, N., Lowe, L. A., Lutter, R., Manta, A., Mazein, A., McEvoy, L., Menzies-Gow, A., Mores, N., Murray, C. S., Nething, K., Nihlen, U., Niven, R., Nordlund, B., Nsubuga, S., Pellet, J., Pison, C., Pratico, G., Puig Valls, M., Riemann, K., Rocha, J. P., Rossios, C., Santini, G., Saqi, M., Scott, S., Sehgal, N., Selby, A., Soderman, P., Sogbesan, A., Spycher, F., Stephan, S., Stokholm, J., Sunther, M., Szentkereszty, M., Tamasi, L., Tariq, K., Valente, S., van Aalderen, W. M., van Drunen, C. M., Van Eyll, J., Vyas, A., Yu, W., Zetterquist, W., Zolkipli, Z., Zwinderman, A. H., Adriaens, Nora, Aliprantis, Antonios, Alving, Kjell, Bakke, Per, Balgoma, David, Barber, Clair, Baribaud, Frederic, Bates, Stewart, Bautmans, An, Beleta, Jorge, Bochenek, Grazyna, Braun, Armin, Carayannopoulos, Leon, Rocha, Joao Pedro Carvalho da Purificacao, Chaleckis, Romanas, D'Amico, Arnaldo, De Alba, Jorge, De Lepeleire, Inge, Dekker, Tamara, Dijkhuis, Annemiek, Draper, Aleksandra, Edwards, Jessica, Emma, Rosalia, Ericsson, Magnus, Flood, Breda, Gallart, Hector, Gomez, Cristina, Gove, Kerry, Gozzard, Neil, Haughney, John, Hewitt, Lorraine, Hohlfeld, Jens, Holweg, Cecile, Hu, Richard, Hu, Sile, Kamphuis, Juliette, Kennington, Erika J., Kerry, Dyson, Knobel, Hugo, Kolmert, Johan, Kots, Maxim, Kuo, Scott, Kupczyk, Maciej, Lambrecht, Bart, Lone-Latif, Saeeda, Loza, Matthew J., Marouzet, Lisa, Martin, Jane, Masefield, Sarah, Mathon, Caroline, Meah, Sally, Meiser, Andrea, Metcalf, Leanne, Mikus, Maria, Miralpeix, Montse, Monk, Philip, Naz, Shama, Nilsson, Peter, Ostling, Jorgen, Pacino, Antonio, Palkonen, Susanna, Pavlidis, Stelios, Pennazza, Giorgio, Petren, Anne, Pink, Sandy, Postle, Anthony, Powell, Pippa, Rahman-Amin, Malayka, Rao, Navin, Ravanetti, Lara, Ray, Emma, Reinke, Stacey, Reynolds, Leanne, Robberechts, Martine, Roberts, Amanda, Russell, Kirsty, Rutgers, Michael, Santoninco, Marco, Schoelch, Corinna, Sjodin, Marcus, Smids, Barbara, Smith, Caroline, Smith, Jessica, Smith, Katherine M., Thorngren, John-Olof, Thornton, Bob, Thorsen, Jonathan, van de Pol, Marianne, van Geest, Marleen, Versnel, Jenny, Vink, Anton, Wald, Frans, Walker, Samantha, Weiszhart, Zsoka, Wetzel, Kristiane, Wheelock, Craig E., Wiegman, Coen, Williams, Sian, Wilson, Susan J., Woodcock, Ashley, Yang, Xian, Yeyasingham, Elizabeth, Prins, Jan-Bas, Gahlemann, Martina, Visintin, Luigi, Evans, Hazel, Puhl, Martine, Buzermaniene, Lina, Hudson, Val, Bond, Laura, de Boer, Pim, Widdershoven, Guy, Sigmund, Ralf, Supple, David, Hamerlijnck, Dominique, Negus, Jenny, Kamphuis, Julitte, Sergison, Lehanne, Onstein, Susanne, MacNee, William, Bernardini, Renato, Bont, Louis, and Wecksell, Per-Ake

Abstract

Background: Stratification by eosinophil and neutrophil counts increases our understanding of asthma and helps target therapy, but there is room for improvement in our accuracy in prediction of treatment responses and a need for better understanding of the underlying mechanisms. Objective: We sought to identify molecular subphenotypes of asthma defined by proteomic signatures for improved stratification. Methods: Unbiased label-free quantitative mass spectrometry and topological data analysis were used to analyze the proteomes of sputum supernatants from 246 participants (206 asthmatic patients) as a novel means of asthma stratification. Microarray analysis of sputum cells provided transcriptomics data additionally to inform on underlying mechanisms. Results: Analysis of the sputum proteome resulted in 10 clusters (ie, proteotypes) based on similarity in proteomic features, representing discrete molecular subphenotypes of asthma. Overlaying granulocyte counts onto the 10 clusters as metadata further defined 3 of these as highly eosinophilic, 3 as highly neutrophilic, and 2 as highly atopic with relatively low granulocytic inflammation. For each of these 3 phenotypes, logistic regression analysis identified candidate protein biomarkers, and matched transcriptomic data pointed to differentially activated underlying mechanisms. Conclusion: This study provides further stratification of asthma currently classified based on quantification of granulocytic inflammation and provided additional insight into their underlying mechanisms, which could become targets for novel therapies.

Published
2019
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