Acute Exacerbations of COPD: Identification of Biological Clusters and Their Biomarkers.

Bafadhel, M., McKenna, S., Terry, S., Mistry, V., Reid, C., Haldar, P., McCormick, M., Haldar, K., Kebadze, T., Duvoix, A., Lindblad, K., Patel, H., Rugman, P., Dodson, P., Jenkins, M., Saunders, M., Newbold, P., Green, R.H., Venge, P., Lomas, D.A., Barer, M.R., Johnston, S.L., Pavord, I.D., Brightling, C.E.
Journal   Am J Respir Crit Care Med.
Species  
Analytes Measured   Troponin I cardiac , Eotaxin-3 , GM-CSF , I-TAC , IL-10 , IL-13 , IL-4 , IL-5 , IL-6 , IL-6R , IL-8 , IP-10 , MCP-1 , MCP-4 , Myoglobin , RANTES , SAA , TARC , TNF-RI , TNF-RII
Matrix Tested   Serum and sputum
Year   2011
Volume  
Page Numbers  
Application   Cytokines and Chemokines
Abstract
Rationale Exacerbations of chronic obstructive pulmonary disease (COPD) are heterogeneous with respect to inflammation and etiology. Objectives Investigate biomarker expression in COPD exacerbations to identify biological clusters and determine biomarkers that recognise clinical COPD exacerbation phenotypes namely those associated with bacteria, viruses or eosinophilic airway inflammation. Methods Patients with COPD were observed for 1 year at stable and exacerbation visits. Biomarkers were measured in sputum and serum. Viruses and selected bacteria were assessed in sputum by polymerase chain reaction and routine diagnostic bacterial culture. Biological phenotypes were explored using unbiased cluster analysis and biomarkers that differentiated clinical exacerbation phenotypes were investigated. Measurements and Main Results 145 patients (101 men, 44 women) entered the study. 182 exacerbations were captured from 86 patients. Four distinct biological exacerbation clusters were identified. These were bacterial, viral or eosinophilic-predominant and a fourth was associated with limited changes in the inflammatory profile and was termed pauci-inflammatory. Of all exacerbations, 55%, 29% and 28% were associated with bacteria, virus and/or a sputum eosinophilia. The biomarkers that best identified these clinical phenotypes were sputum IL-1β (area under receiver-operator-characteristic-curve 0.89 (95% confidence interval 0.83 to 0.95), serum CXCL10 0.83 (0.70 to 0.96), and percentage peripheral eosinophils 0.85 (0.78 to 0.93) respectively. Conclusion The heterogeneity of the biological response of COPD exacerbations can be defined. Sputum IL-1β, serum CXCL10 and peripheral eosinophils are biomarkers of bacteria, virus or eosinophil associated exacerbations of COPD. Whether phenotype-specific biomarkers can be applied to direct therapy warrants further investigation.

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U-PLEX Mouse IL-10 Assay
IL-10 | Mouse
Singleplex
U-PLEX Mouse IL-13 Assay
IL-13 | Mouse
Singleplex
U-PLEX NHP Eotaxin-3 Assay
Eotaxin-3 | Non-human primate
Singleplex
U-PLEX NHP GM-CSF Assay
GM-CSF | Non-human primate
Singleplex
U-PLEX NHP IL-5 Assay
IL-5 | Non-human primate
Singleplex
U-PLEX NHP IL-6 Assay
IL-6 | Non-human primate
Singleplex
U-PLEX NHP IL-8 Assay
IL-8 | Non-human primate
Singleplex
U-PLEX NHP IL-10 Assay
IL-10 | Non-human primate
Singleplex
U-PLEX NHP IP-10 Assay
IP-10 | Non-human primate
Singleplex
U-PLEX NHP I-TAC Assay
I-TAC | Non-human primate
Singleplex
U-PLEX NHP MCP-1 Assay
MCP-1 | Non-human primate
Singleplex
U-PLEX NHP MCP-4 Assay
MCP-4 | Non-human primate
Singleplex
U-PLEX NHP TARC Assay
TARC | Non-human primate
Singleplex
U-PLEX Proinflam Combo 1 Human
IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, TNF-α | Human
Multiplex
U-PLEX Proinflam Combo 1 NHP
IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12/IL-23p40, TNF-α | Non-human primate
Multiplex
U-PLEX Proinflam Combo 2 Human
GM-CSF, IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70 | Human
Multiplex
U-PLEX Proinflam Combo 3 Human
IFN-γ, IL-1β, IL-6, TNF-α | Human
Multiplex
U-PLEX Proinflam Combo 4 Human
IL-1β, IL-6, IL-8, TNF-α | Human
Multiplex
U-PLEX TH1/TH2 Combo Human
IFN-γ, IL-1β, IL-2, IL-4, IL-5, IL-8, IL-10, IL-12p70, IL-13, TNF-α | Human
Multiplex
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