Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort
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...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Uruj Hoda [verfasserIn] Stelios Pavlidis [verfasserIn] Aruna T. Bansal [verfasserIn] Kentaro Takahashi [verfasserIn] Sile Hu [verfasserIn] Francois Ng Kee Kwong [verfasserIn] Christos Rossios [verfasserIn] Kai Sun [verfasserIn] Pankaj Bhavsar [verfasserIn] Matthew Loza [verfasserIn] Frederic Baribaud [verfasserIn] Pascal Chanez [verfasserIn] Stephen J. Fowler [verfasserIn] Ildiko Horvath [verfasserIn] Paolo Montuschi [verfasserIn] Florian Singer [verfasserIn] Jacek Musial [verfasserIn] Barbro Dahlen [verfasserIn] Norbert Krug [verfasserIn] Thomas Sandstrom [verfasserIn] Dominic E. Shaw [verfasserIn] Rene Lutter [verfasserIn] Louise J. Fleming [verfasserIn] Peter H. Howarth [verfasserIn] Massimo Caruso [verfasserIn] Ana R. Sousa [verfasserIn] Julie Corfield [verfasserIn] Charles Auffray [verfasserIn] Bertrand De Meulder [verfasserIn] Diane Lefaudeux [verfasserIn] Sven‐Erik Dahlen [verfasserIn] Ratko Djukanovic [verfasserIn] Peter J. Sterk [verfasserIn] Yike Guo [verfasserIn] Ian M. Adcock [verfasserIn] Kian Fan Chung [verfasserIn] the U‐BIOPRED study group [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Übergeordnetes Werk: |
In: Clinical and Translational Medicine - Wiley, 2013, 12(2022), 4, Seite n/a-n/a |
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| Übergeordnetes Werk: |
volume:12 ; year:2022 ; number:4 ; pages:n/a-n/a |
| Links: |
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| DOI / URN: |
10.1002/ctm2.816 |
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| Katalog-ID: |
DOAJ02508013X |
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| 245 | 1 | 0 | |a Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort |
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| 520 | |a 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. | ||
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10.1002/ctm2.816 doi (DE-627)DOAJ02508013X (DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da DE-627 ger DE-627 rakwb eng R5-920 Uruj Hoda verfasserin aut Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. asthma exacerbations severe asthma CEACAM5 frequent exacerbators persistent frequent exacerbators Medicine (General) Stelios Pavlidis verfasserin aut Aruna T. Bansal verfasserin aut Kentaro Takahashi verfasserin aut Sile Hu verfasserin aut Francois Ng Kee Kwong verfasserin aut Christos Rossios verfasserin aut Kai Sun verfasserin aut Pankaj Bhavsar verfasserin aut Matthew Loza verfasserin aut Frederic Baribaud verfasserin aut Pascal Chanez verfasserin aut Stephen J. Fowler verfasserin aut Ildiko Horvath verfasserin aut Paolo Montuschi verfasserin aut Florian Singer verfasserin aut Jacek Musial verfasserin aut Barbro Dahlen verfasserin aut Norbert Krug verfasserin aut Thomas Sandstrom verfasserin aut Dominic E. Shaw verfasserin aut Rene Lutter verfasserin aut Louise J. Fleming verfasserin aut Peter H. Howarth verfasserin aut Massimo Caruso verfasserin aut Ana R. Sousa verfasserin aut Julie Corfield verfasserin aut Charles Auffray verfasserin aut Bertrand De Meulder verfasserin aut Diane Lefaudeux verfasserin aut Sven‐Erik Dahlen verfasserin aut Ratko Djukanovic verfasserin aut Peter J. Sterk verfasserin aut Yike Guo verfasserin aut Ian M. Adcock verfasserin aut Kian Fan Chung verfasserin aut the U‐BIOPRED study group verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 4, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:4 pages:n/a-n/a https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/article/472cffbdc9ba4c16ac2d4d6cd89330da kostenfrei https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2022 4 n/a-n/a |
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10.1002/ctm2.816 doi (DE-627)DOAJ02508013X (DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da DE-627 ger DE-627 rakwb eng R5-920 Uruj Hoda verfasserin aut Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. asthma exacerbations severe asthma CEACAM5 frequent exacerbators persistent frequent exacerbators Medicine (General) Stelios Pavlidis verfasserin aut Aruna T. Bansal verfasserin aut Kentaro Takahashi verfasserin aut Sile Hu verfasserin aut Francois Ng Kee Kwong verfasserin aut Christos Rossios verfasserin aut Kai Sun verfasserin aut Pankaj Bhavsar verfasserin aut Matthew Loza verfasserin aut Frederic Baribaud verfasserin aut Pascal Chanez verfasserin aut Stephen J. Fowler verfasserin aut Ildiko Horvath verfasserin aut Paolo Montuschi verfasserin aut Florian Singer verfasserin aut Jacek Musial verfasserin aut Barbro Dahlen verfasserin aut Norbert Krug verfasserin aut Thomas Sandstrom verfasserin aut Dominic E. Shaw verfasserin aut Rene Lutter verfasserin aut Louise J. Fleming verfasserin aut Peter H. Howarth verfasserin aut Massimo Caruso verfasserin aut Ana R. Sousa verfasserin aut Julie Corfield verfasserin aut Charles Auffray verfasserin aut Bertrand De Meulder verfasserin aut Diane Lefaudeux verfasserin aut Sven‐Erik Dahlen verfasserin aut Ratko Djukanovic verfasserin aut Peter J. Sterk verfasserin aut Yike Guo verfasserin aut Ian M. Adcock verfasserin aut Kian Fan Chung verfasserin aut the U‐BIOPRED study group verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 4, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:4 pages:n/a-n/a https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/article/472cffbdc9ba4c16ac2d4d6cd89330da kostenfrei https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2022 4 n/a-n/a |
| allfields_unstemmed |
10.1002/ctm2.816 doi (DE-627)DOAJ02508013X (DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da DE-627 ger DE-627 rakwb eng R5-920 Uruj Hoda verfasserin aut Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. asthma exacerbations severe asthma CEACAM5 frequent exacerbators persistent frequent exacerbators Medicine (General) Stelios Pavlidis verfasserin aut Aruna T. Bansal verfasserin aut Kentaro Takahashi verfasserin aut Sile Hu verfasserin aut Francois Ng Kee Kwong verfasserin aut Christos Rossios verfasserin aut Kai Sun verfasserin aut Pankaj Bhavsar verfasserin aut Matthew Loza verfasserin aut Frederic Baribaud verfasserin aut Pascal Chanez verfasserin aut Stephen J. Fowler verfasserin aut Ildiko Horvath verfasserin aut Paolo Montuschi verfasserin aut Florian Singer verfasserin aut Jacek Musial verfasserin aut Barbro Dahlen verfasserin aut Norbert Krug verfasserin aut Thomas Sandstrom verfasserin aut Dominic E. Shaw verfasserin aut Rene Lutter verfasserin aut Louise J. Fleming verfasserin aut Peter H. Howarth verfasserin aut Massimo Caruso verfasserin aut Ana R. Sousa verfasserin aut Julie Corfield verfasserin aut Charles Auffray verfasserin aut Bertrand De Meulder verfasserin aut Diane Lefaudeux verfasserin aut Sven‐Erik Dahlen verfasserin aut Ratko Djukanovic verfasserin aut Peter J. Sterk verfasserin aut Yike Guo verfasserin aut Ian M. Adcock verfasserin aut Kian Fan Chung verfasserin aut the U‐BIOPRED study group verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 4, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:4 pages:n/a-n/a https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/article/472cffbdc9ba4c16ac2d4d6cd89330da kostenfrei https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2022 4 n/a-n/a |
| allfieldsGer |
10.1002/ctm2.816 doi (DE-627)DOAJ02508013X (DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da DE-627 ger DE-627 rakwb eng R5-920 Uruj Hoda verfasserin aut Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. asthma exacerbations severe asthma CEACAM5 frequent exacerbators persistent frequent exacerbators Medicine (General) Stelios Pavlidis verfasserin aut Aruna T. Bansal verfasserin aut Kentaro Takahashi verfasserin aut Sile Hu verfasserin aut Francois Ng Kee Kwong verfasserin aut Christos Rossios verfasserin aut Kai Sun verfasserin aut Pankaj Bhavsar verfasserin aut Matthew Loza verfasserin aut Frederic Baribaud verfasserin aut Pascal Chanez verfasserin aut Stephen J. Fowler verfasserin aut Ildiko Horvath verfasserin aut Paolo Montuschi verfasserin aut Florian Singer verfasserin aut Jacek Musial verfasserin aut Barbro Dahlen verfasserin aut Norbert Krug verfasserin aut Thomas Sandstrom verfasserin aut Dominic E. Shaw verfasserin aut Rene Lutter verfasserin aut Louise J. Fleming verfasserin aut Peter H. Howarth verfasserin aut Massimo Caruso verfasserin aut Ana R. Sousa verfasserin aut Julie Corfield verfasserin aut Charles Auffray verfasserin aut Bertrand De Meulder verfasserin aut Diane Lefaudeux verfasserin aut Sven‐Erik Dahlen verfasserin aut Ratko Djukanovic verfasserin aut Peter J. Sterk verfasserin aut Yike Guo verfasserin aut Ian M. Adcock verfasserin aut Kian Fan Chung verfasserin aut the U‐BIOPRED study group verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 4, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:4 pages:n/a-n/a https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/article/472cffbdc9ba4c16ac2d4d6cd89330da kostenfrei https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2022 4 n/a-n/a |
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10.1002/ctm2.816 doi (DE-627)DOAJ02508013X (DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da DE-627 ger DE-627 rakwb eng R5-920 Uruj Hoda verfasserin aut Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. asthma exacerbations severe asthma CEACAM5 frequent exacerbators persistent frequent exacerbators Medicine (General) Stelios Pavlidis verfasserin aut Aruna T. Bansal verfasserin aut Kentaro Takahashi verfasserin aut Sile Hu verfasserin aut Francois Ng Kee Kwong verfasserin aut Christos Rossios verfasserin aut Kai Sun verfasserin aut Pankaj Bhavsar verfasserin aut Matthew Loza verfasserin aut Frederic Baribaud verfasserin aut Pascal Chanez verfasserin aut Stephen J. Fowler verfasserin aut Ildiko Horvath verfasserin aut Paolo Montuschi verfasserin aut Florian Singer verfasserin aut Jacek Musial verfasserin aut Barbro Dahlen verfasserin aut Norbert Krug verfasserin aut Thomas Sandstrom verfasserin aut Dominic E. Shaw verfasserin aut Rene Lutter verfasserin aut Louise J. Fleming verfasserin aut Peter H. Howarth verfasserin aut Massimo Caruso verfasserin aut Ana R. Sousa verfasserin aut Julie Corfield verfasserin aut Charles Auffray verfasserin aut Bertrand De Meulder verfasserin aut Diane Lefaudeux verfasserin aut Sven‐Erik Dahlen verfasserin aut Ratko Djukanovic verfasserin aut Peter J. Sterk verfasserin aut Yike Guo verfasserin aut Ian M. Adcock verfasserin aut Kian Fan Chung verfasserin aut the U‐BIOPRED study group verfasserin aut In Clinical and Translational Medicine Wiley, 2013 12(2022), 4, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:12 year:2022 number:4 pages:n/a-n/a https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/article/472cffbdc9ba4c16ac2d4d6cd89330da kostenfrei https://doi.org/10.1002/ctm2.816 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2022 4 n/a-n/a |
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Uruj Hoda @@aut@@ Stelios Pavlidis @@aut@@ Aruna T. Bansal @@aut@@ Kentaro Takahashi @@aut@@ Sile Hu @@aut@@ Francois Ng Kee Kwong @@aut@@ Christos Rossios @@aut@@ Kai Sun @@aut@@ Pankaj Bhavsar @@aut@@ Matthew Loza @@aut@@ Frederic Baribaud @@aut@@ Pascal Chanez @@aut@@ Stephen J. Fowler @@aut@@ Ildiko Horvath @@aut@@ Paolo Montuschi @@aut@@ Florian Singer @@aut@@ Jacek Musial @@aut@@ Barbro Dahlen @@aut@@ Norbert Krug @@aut@@ Thomas Sandstrom @@aut@@ Dominic E. Shaw @@aut@@ Rene Lutter @@aut@@ Louise J. Fleming @@aut@@ Peter H. Howarth @@aut@@ Massimo Caruso @@aut@@ Ana R. Sousa @@aut@@ Julie Corfield @@aut@@ Charles Auffray @@aut@@ Bertrand De Meulder @@aut@@ Diane Lefaudeux @@aut@@ Sven‐Erik Dahlen @@aut@@ Ratko Djukanovic @@aut@@ Peter J. Sterk @@aut@@ Yike Guo @@aut@@ Ian M. Adcock @@aut@@ Kian Fan Chung @@aut@@ the U‐BIOPRED study group @@aut@@ |
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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. 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Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort |
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Uruj Hoda Stelios Pavlidis Aruna T. Bansal Kentaro Takahashi Sile Hu Francois Ng Kee Kwong Christos Rossios Kai Sun Pankaj Bhavsar Matthew Loza Frederic Baribaud Pascal Chanez Stephen J. Fowler Ildiko Horvath Paolo Montuschi Florian Singer Jacek Musial Barbro Dahlen Norbert Krug Thomas Sandstrom Dominic E. Shaw Rene Lutter Louise J. Fleming Peter H. Howarth Massimo Caruso Ana R. Sousa Julie Corfield Charles Auffray Bertrand De Meulder Diane Lefaudeux Sven‐Erik Dahlen Ratko Djukanovic Peter J. Sterk Yike Guo Ian M. Adcock Kian Fan Chung the U‐BIOPRED study group |
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clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in u‐biopred cohort |
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R5-920 |
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Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort |
| abstract |
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. |
| abstractGer |
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. |
| abstract_unstemmed |
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. |
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Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ02508013X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230307082946.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ctm2.816</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ02508013X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ472cffbdc9ba4c16ac2d4d6cd89330da</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">R5-920</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Uruj Hoda</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Clinical and transcriptomic features of persistent exacerbation‐prone severe asthma in U‐BIOPRED cohort</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">asthma exacerbations</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">severe asthma</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CEACAM5</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">frequent exacerbators</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">persistent frequent exacerbators</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Medicine (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Stelios Pavlidis</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Aruna T. 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