Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.

BACKGROUND: Asthma and chronic obstructive pulmonary disease (COPD) display features of overlap in airway physiology and airway inflammation. Whether inflammatory phenotypes in airway disease describe similar mediator expression is unknown. OBJECTIVES: To explore the relationship of airway inflammat...

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Main Authors: Bafadhel, M, McCormick, M, Saha, S, McKenna, S, Shelley, M, Hargadon, B, Mistry, V, Reid, C, Parker, D, Dodson, P, Jenkins, M, Lloyd, A, Rugman, P, Newbold, P, Brightling, C
Format: Journal article
Language:English
Published: 2012
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author Bafadhel, M
McCormick, M
Saha, S
McKenna, S
Shelley, M
Hargadon, B
Mistry, V
Reid, C
Parker, D
Dodson, P
Jenkins, M
Lloyd, A
Rugman, P
Newbold, P
Brightling, C
author_facet Bafadhel, M
McCormick, M
Saha, S
McKenna, S
Shelley, M
Hargadon, B
Mistry, V
Reid, C
Parker, D
Dodson, P
Jenkins, M
Lloyd, A
Rugman, P
Newbold, P
Brightling, C
author_sort Bafadhel, M
collection OXFORD
description BACKGROUND: Asthma and chronic obstructive pulmonary disease (COPD) display features of overlap in airway physiology and airway inflammation. Whether inflammatory phenotypes in airway disease describe similar mediator expression is unknown. OBJECTIVES: To explore the relationship of airway inflammation and cytokine and chemokine expression in asthma and COPD. METHODS: Subjects with asthma and COPD (n = 54 and n = 49) were studied. Clinical characteristics and sputum were collected at entry into the study. A 2-step sputum processing method was performed for supernatant and cytospin preparation. Meso Scale Discovery and Luminex platforms were used to measure cytokines, chemokines and matrix metalloproteinase levels. RESULTS: Analytes sensitive to dithiothreitol (DTT) that had increased recovery in the 2-step sputum process were IL-1β, 4, 5, 10, 13, IFN-γ, TNFRI, GM-CSF, CCL2, 3, 4, 5, 13 and 17. There was a differential expression in IL-8, TNFRI and TNFRII between asthma and COPD [mean fold difference (95% CI): IL-8, 2.6 (1.3-5.4), p = 0.01; TNFRI, 2.1 (1.3-5.4), p = 0.03; TNFRII, 2.6 (1.2-5.6), p = 0.02]. In neutrophilic and eosinophilic airway inflammation, TNFα, TNFRI, TNFRII, IL-6, IL-8 and IL-5 could differentiate between these phenotypes. However, these phenotypes were unrelated to the diagnosis of asthma or COPD. CONCLUSION: Recovery of sputum mediators sensitive to DTT can be improved using the described sputum processing technique. Within airway inflammatory sub-phenotypes there is a differential pattern of mediator expression that is independent of disease. Whether these inflammatory phenotypes in asthma and COPD confer distinct pathogeneses, therapeutic responses and clinical phenotypes needs to be further evaluated.
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spelling oxford-uuid:835c1f13-d9bf-45b8-8677-9441e8041b552022-03-26T21:43:43ZProfiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:835c1f13-d9bf-45b8-8677-9441e8041b55EnglishSymplectic Elements at Oxford2012Bafadhel, MMcCormick, MSaha, SMcKenna, SShelley, MHargadon, BMistry, VReid, CParker, DDodson, PJenkins, MLloyd, ARugman, PNewbold, PBrightling, CBACKGROUND: Asthma and chronic obstructive pulmonary disease (COPD) display features of overlap in airway physiology and airway inflammation. Whether inflammatory phenotypes in airway disease describe similar mediator expression is unknown. OBJECTIVES: To explore the relationship of airway inflammation and cytokine and chemokine expression in asthma and COPD. METHODS: Subjects with asthma and COPD (n = 54 and n = 49) were studied. Clinical characteristics and sputum were collected at entry into the study. A 2-step sputum processing method was performed for supernatant and cytospin preparation. Meso Scale Discovery and Luminex platforms were used to measure cytokines, chemokines and matrix metalloproteinase levels. RESULTS: Analytes sensitive to dithiothreitol (DTT) that had increased recovery in the 2-step sputum process were IL-1β, 4, 5, 10, 13, IFN-γ, TNFRI, GM-CSF, CCL2, 3, 4, 5, 13 and 17. There was a differential expression in IL-8, TNFRI and TNFRII between asthma and COPD [mean fold difference (95% CI): IL-8, 2.6 (1.3-5.4), p = 0.01; TNFRI, 2.1 (1.3-5.4), p = 0.03; TNFRII, 2.6 (1.2-5.6), p = 0.02]. In neutrophilic and eosinophilic airway inflammation, TNFα, TNFRI, TNFRII, IL-6, IL-8 and IL-5 could differentiate between these phenotypes. However, these phenotypes were unrelated to the diagnosis of asthma or COPD. CONCLUSION: Recovery of sputum mediators sensitive to DTT can be improved using the described sputum processing technique. Within airway inflammatory sub-phenotypes there is a differential pattern of mediator expression that is independent of disease. Whether these inflammatory phenotypes in asthma and COPD confer distinct pathogeneses, therapeutic responses and clinical phenotypes needs to be further evaluated.
spellingShingle Bafadhel, M
McCormick, M
Saha, S
McKenna, S
Shelley, M
Hargadon, B
Mistry, V
Reid, C
Parker, D
Dodson, P
Jenkins, M
Lloyd, A
Rugman, P
Newbold, P
Brightling, C
Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title_full Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title_fullStr Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title_full_unstemmed Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title_short Profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease.
title_sort profiling of sputum inflammatory mediators in asthma and chronic obstructive pulmonary disease
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