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

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 CE.
Journal   Respiration.
Species  
Analytes Measured   Eotaxin , I-TAC , IL-5 , IL-6 , IL-6R , IL-8 , IP-10 , MCP-1 , MCP-4 , MMP-8 , MMP-9 , RANTES , TARC , TNF-RI , TNF-RII , Flt-1 VEGFR1
Matrix Tested   Sputum
Year   2012
Volume   83
Page Numbers   36-44
Application   Cytokines and Chemokines
Abstract
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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Singleplex
U-PLEX Mouse IL-6 Assay
IL-6 | Mouse
Singleplex
U-PLEX NHP TARC Antibody Set
TARC | Non-human primate
U-PLEX Chemokine Combo 1 NHP
Eotaxin, Eotaxin-3, IL-8, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, TARC | Non-human primate
Multiplex
U-PLEX Cytokine Combo 1 NHP
GM-CSF, IL-1α, IL-5, IL-7, IL-12/IL-23p40, IL-15, IL-16, IL-17A, TNF-β, VEGF-A | Non-human primate
Multiplex
U-PLEX Human Eotaxin Assay
Eotaxin | Human
Singleplex
U-PLEX Human IL-5 Assay
IL-5 | Human
Singleplex
U-PLEX Human IL-6 Assay
IL-6 | Human
Singleplex
U-PLEX Human TARC Antibody Set
TARC | Human
U-PLEX Mouse IL-5 Antibody Set
IL-5 | Mouse
U-PLEX Mouse IL-6 Antibody Set
IL-6 | Mouse
U-PLEX NHP IL-5 Antibody Set
IL-5 | Non-human primate
U-PLEX NHP IL-6 Antibody Set
IL-6 | Non-human primate
U-PLEX NHP IL-8 Antibody Set
IL-8 | Non-human primate
U-PLEX NHP IP-10 Antibody Set
IP-10 | Non-human primate
U-PLEX NHP I-TAC Antibody Set
I-TAC | Non-human primate
U-PLEX NHP MCP-1 Antibody Set
MCP-1 | Non-human primate
U-PLEX NHP MCP-4 Antibody Set
MCP-4 | Non-human primate
U-PLEX Human Eotaxin Antibody Set
Eotaxin | Human
U-PLEX Human IL-5 Antibody Set
IL-5 | Human
U-PLEX Human IL-6 Antibody Set
IL-6 | Human
U-PLEX Human IL-8 Antibody Set
IL-8 | Human
U-PLEX Human IP-10 Antibody Set
IP-10 | Human
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