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3 results on '"De Meulder, Bertrand"'

1. COVID19 Disease Map, a computational knowledge repository of virus-host interaction mechanisms

Author

Ostaszewski, Marek, Niarakis, Anna, Mazein, Alexander, Kuperstein, Inna, Phair, Robert, Orta-Resendiz, Aurelio, Singh, Vidisha, Aghamiri, Sara Sadat, Acencio, Marcio Luis, Glaab, Enrico, Ruepp, Andreas, Fobo, Gisela, Montrone, Corinna, Brauner, Barbara, Frishman, Goar, Gomez, Luis Cristobal Monraz, Somers, Julia, Hoch, Matti, Gupta, Shailendra Kumar, Scheel, Julia, Borlinghaus, Hanna, Czauderna, Tobias, Schreiber, Falk, Montagud, Arnau, de Leon, Miguel Ponce, Funahashi, Akira, Hiki, Yusuke, Hiroi, Noriko, Yamada, Takahiro G., Draeger, Andreas, Renz, Alina, Naveez, Muhammad, Bocskei, Zsolt, Messina, Francesco, Boernigen, Daniela, Fergusson, Liam, Conti, Marta, Rameil, Marius, Nakonecnij, Vanessa, Vanhoefer, Jakob, Schmiester, Leonard, Wang, Muying, Ackerman, Emily E., Shoemaker, Jason E., Zucker, Jeremy, Oxford, Kristie, Teuton, Jeremy, Kocakaya, Ebru, Summak, Gokce Yagmur, Hanspers, Kristina, Kutmon, Martina, Coort, Susan, Eijssen, Lars, Ehrhart, Friederike, Rex, Devasahayam Arokia Balaya, Slenter, Denise, Martens, Marvin, Pham, Nhung, Haw, Robin, Jassal, Bijay, Matthews, Lisa, Orlic-Milacic, Marija, Ribeiro, Andrea Senff, Rothfels, Karen, Shamovsky, Veronica, Stephan, Ralf, Sevilla, Cristoffer, Varusai, Thawfeek, Ravel, Jean-Marie, Fraser, Rupsha, Ortseifen, Vera, Marchesi, Silvia, Gawron, Piotr, Smula, Ewa, Heirendt, Laurent, Satagopam, Venkata, Wu, Guanming, Riutta, Anders, Golebiewski, Martin, Owen, Stuart, Goble, Carole, Hu, Xiaoming, Overall, Rupert W., Maier, Dieter, Bauch, Angela, Gyori, Benjamin M., Bachman, John A., Vega, Carlos, Groues, Valentin, Vazquez, Miguel, Porras, Pablo, Licata, Luana, Iannuccelli, Marta, Sacco, Francesca, Nesterova, Anastasia, Yuryev, Anton, de Waard, Anita, Turei, Denes, Luna, Augustin, Babur, Ozgun, Soliman, Sylvain, Valdeolivas, Alberto, Esteban-Medina, Marina, Pena-Chilet, Maria, Rian, Kinza, Helikar, Tomas, Puniya, Bhanwar Lal, Modos, Dezso, Treveil, Agatha, Olbei, Marton, De Meulder, Bertrand, Ballereau, Stephane, Dugourd, Aurelien, Naldi, Aurelien, Noel, Vincent, Calzone, Laurence, Sander, Chris, Demir, Emek, Korcsmaros, Tamas, Freeman, Tom C., Auge, Franck, Beckmann, Jacques S., Hasenauer, Jan, Wolkenhauer, Olaf, Wilighagen, Egon L., Pico, Alexander R., Evelo, Chris T., Gillespie, Marc E., Stein, Lincoln D., Hermjakob, Henning, D'Eustachio, Peter, Saez-Rodriguez, Julio, Dopazo, Joaquin, Valencia, Alfonso, Kitano, Hiroaki, Barillot, Emmanuel, Auffray, Charles, Balling, Rudi, Schneider, Reinhard, Ostaszewski, Marek, Niarakis, Anna, Mazein, Alexander, Kuperstein, Inna, Phair, Robert, Orta-Resendiz, Aurelio, Singh, Vidisha, Aghamiri, Sara Sadat, Acencio, Marcio Luis, Glaab, Enrico, Ruepp, Andreas, Fobo, Gisela, Montrone, Corinna, Brauner, Barbara, Frishman, Goar, Gomez, Luis Cristobal Monraz, Somers, Julia, Hoch, Matti, Gupta, Shailendra Kumar, Scheel, Julia, Borlinghaus, Hanna, Czauderna, Tobias, Schreiber, Falk, Montagud, Arnau, de Leon, Miguel Ponce, Funahashi, Akira, Hiki, Yusuke, Hiroi, Noriko, Yamada, Takahiro G., Draeger, Andreas, Renz, Alina, Naveez, Muhammad, Bocskei, Zsolt, Messina, Francesco, Boernigen, Daniela, Fergusson, Liam, Conti, Marta, Rameil, Marius, Nakonecnij, Vanessa, Vanhoefer, Jakob, Schmiester, Leonard, Wang, Muying, Ackerman, Emily E., Shoemaker, Jason E., Zucker, Jeremy, Oxford, Kristie, Teuton, Jeremy, Kocakaya, Ebru, Summak, Gokce Yagmur, Hanspers, Kristina, Kutmon, Martina, Coort, Susan, Eijssen, Lars, Ehrhart, Friederike, Rex, Devasahayam Arokia Balaya, Slenter, Denise, Martens, Marvin, Pham, Nhung, Haw, Robin, Jassal, Bijay, Matthews, Lisa, Orlic-Milacic, Marija, Ribeiro, Andrea Senff, Rothfels, Karen, Shamovsky, Veronica, Stephan, Ralf, Sevilla, Cristoffer, Varusai, Thawfeek, Ravel, Jean-Marie, Fraser, Rupsha, Ortseifen, Vera, Marchesi, Silvia, Gawron, Piotr, Smula, Ewa, Heirendt, Laurent, Satagopam, Venkata, Wu, Guanming, Riutta, Anders, Golebiewski, Martin, Owen, Stuart, Goble, Carole, Hu, Xiaoming, Overall, Rupert W., Maier, Dieter, Bauch, Angela, Gyori, Benjamin M., Bachman, John A., Vega, Carlos, Groues, Valentin, Vazquez, Miguel, Porras, Pablo, Licata, Luana, Iannuccelli, Marta, Sacco, Francesca, Nesterova, Anastasia, Yuryev, Anton, de Waard, Anita, Turei, Denes, Luna, Augustin, Babur, Ozgun, Soliman, Sylvain, Valdeolivas, Alberto, Esteban-Medina, Marina, Pena-Chilet, Maria, Rian, Kinza, Helikar, Tomas, Puniya, Bhanwar Lal, Modos, Dezso, Treveil, Agatha, Olbei, Marton, De Meulder, Bertrand, Ballereau, Stephane, Dugourd, Aurelien, Naldi, Aurelien, Noel, Vincent, Calzone, Laurence, Sander, Chris, Demir, Emek, Korcsmaros, Tamas, Freeman, Tom C., Auge, Franck, Beckmann, Jacques S., Hasenauer, Jan, Wolkenhauer, Olaf, Wilighagen, Egon L., Pico, Alexander R., Evelo, Chris T., Gillespie, Marc E., Stein, Lincoln D., Hermjakob, Henning, D'Eustachio, Peter, Saez-Rodriguez, Julio, Dopazo, Joaquin, Valencia, Alfonso, Kitano, Hiroaki, Barillot, Emmanuel, Auffray, Charles, Balling, Rudi, and Schneider, Reinhard

Abstract

We need to effectively combine the knowledge from surging literature with complex datasets to propose mechanistic models of SARS-CoV-2 infection, improving data interpretation and predicting key targets of intervention. Here, we describe a large-scale community effort to build an open access, interoperable and computable repository of COVID-19 molecular mechanisms. The COVID-19 Disease Map (C19DMap) is a graphical, interactive representation of disease-relevant molecular mechanisms linking many knowledge sources. Notably, it is a computational resource for graph-based analyses and disease modelling. To this end, we established a framework of tools, platforms and guidelines necessary for a multifaceted community of biocurators, domain experts, bioinformaticians and computational biologists. The diagrams of the C19DMap, curated from the literature, are integrated with relevant interaction and text mining databases. We demonstrate the application of network analysis and modelling approaches by concrete examples to highlight new testable hypotheses. This framework helps to find signatures of SARS-CoV-2 predisposition, treatment response or prioritisation of drug candidates. Such an approach may help deal with new waves of COVID-19 or similar pandemics in the long-term perspective.

Published
2021
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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. Clinical and transcriptomic features of persistent exacerbation-prone severe asthma in U-BIOPRED cohort.

Author

Hoda U, Pavlidis S, Bansal AT, Takahashi K, Hu S, Ng Kee Kwong F, Rossios C, Sun K, Bhavsar P, Loza M, Baribaud F, Chanez P, Fowler SJ, Horvath I, Montuschi P, Singer F, Musial J, Dahlen B, Krug N, Sandstrom T, Shaw DE, Lutter R, Fleming LJ, Howarth PH, Caruso M, Sousa AR, Corfield J, Auffray C, De Meulder B, Lefaudeux D, Dahlen SE, Djukanovic R, Sterk PJ, Guo Y, Adcock IM, and Chung KF

Subjects
Bronchi pathology, Cohort Studies, Humans, Sputum metabolism, Asthma genetics, Asthma metabolism, Asthma pathology, Transcriptome genetics
Abstract

Background: Exacerbation-prone asthma is a feature of severe disease. However, the basis for its persistency remains unclear., Objectives: To determine the clinical and transcriptomic features of frequent exacerbators (FEs) and persistent FEs (PFEs) in the U-BIOPRED cohort., Methods: We compared features of FE (≥2 exacerbations in past year) to infrequent exacerbators (IE, <2 exacerbations) and of PFE with repeat ≥2 exacerbations during the following year to persistent IE (PIE). Transcriptomic data in blood, bronchial and nasal epithelial brushings, bronchial biopsies and sputum cells were analysed by gene set variation analysis for 103 gene signatures., Results: Of 317 patients, 62.4% had FE, of whom 63.6% had PFE, while 37.6% had IE, of whom 61.3% had PIE. Using multivariate analysis, FE was associated with short-acting beta-agonist use, sinusitis and daily oral corticosteroid use, while PFE was associated with eczema, short-acting beta-agonist use and asthma control index. CEA cell adhesion molecule 5 (CEACAM5) was the only differentially expressed transcript in bronchial biopsies between PE and IE. There were no differentially expressed genes in the other four compartments. There were higher expression scores for type 2, T-helper type-17 and type 1 pathway signatures together with those associated with viral infections in bronchial biopsies from FE compared to IE, while there were higher expression scores of type 2, type 1 and steroid insensitivity pathway signatures in bronchial biopsies of PFE compared to PIE., Conclusion: The FE group and its PFE subgroup are associated with poor asthma control while expressing higher type 1 and type 2 activation pathways compared to IE and PIE, respectively., (© 2022 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.)

Published
2022
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