Blood MCP-1 levels are increased in chronic obstructive pulmonary disease patients with prevalent emphysema
Authors Di Stefano A, Coccini T, Roda E, Signorini C, Balbi B, Brunetti G, Ceriana P
Received 14 December 2017
Accepted for publication 12 March 2018
Published 24 May 2018 Volume 2018:13 Pages 1691—1700
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Richard Russell
Antonino Di Stefano,1 Teresa Coccini,2 Elisa Roda,2 Cinzia Signorini,3 Bruno Balbi,1 Giuseppe Brunetti,4 Piero Ceriana4
1Pulmonary Rehabilitation Unit and Laboratory of Cytoimmunopathology of the Heart and Lung, Istituti Clinici Scientifici Maugeri SpA Società Benefit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Veruno, Italy; 2Laboratory of Experimental and Clinical Toxicology, Toxicology Unit, ICS Maugeri SpA Società Benefit, Istituto di Ricovero e Cura a Carattere Scientifico, Pavia, Italy; 3Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy; 4Pulmonary Rehabilitation Unit, Istituti Clinici Scientifici Maugeri SpA Società Benefit, Istituto di Ricovero e Cura a Carattere Scientifico, Pavia, Italy
Background and aims: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by different phenotypes with either bronchial airways alterations or emphysema prevailing. As blood biomarkers could be clinically useful for COPD stratification, we aimed at investigating the levels of blood biomarkers in COPD patients differentiated by phenotype: prevalent chronic airway disease versus emphysema.
Methods: In 23 COPD patients with prevalent airway disease (COPD-B), 22 COPD patients with prevalent emphysema (COPD-E), 9 control smokers (CSs), and 18 control nonsmokers (CNSs), we analyzed the expression levels of interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, epidermal growth factor (EGF), monocyte chemotactic protein (MCP)-1, and vascular endothelial growth factor by enzyme-linked immunosorbent assay in plasma/serum; glutathione peroxidase and superoxide dismutase (SOD)-1 by immunochemical kits in plasma; and free F2-isoprostanes (F2-IsoPs) by gas chromatography in plasma.
Results: F2-IsoPs level was increased in COPD-B and COPD-E compared with CSs and CNSs; in addition, CS showed higher levels than CNSs; SOD1 level was lower in COPD-B and COPD-E than that in CNSs. Interestingly, MCP-1 level was higher only in COPD-E versus CSs and CNSs; EGF and IL-8 levels were higher in COPD-B and COPD-E versus CNSs; IL-6 level was increased in all three smoking groups (COPD-B, COPD-E, and CSs) versus CNS; IFN-γ and IL-1α levels were higher in CSs than in CNSs; and IL-1α level was also higher in CSs versus COPD-B and COPD-E. In all subjects, F2-IsoPs level correlated positively and significantly with MCP-1, IL-2, IL-1β, IFN-γ, and TNF-α and negatively with SOD1. When correlations were restricted to COPD-E and COPD-B groups, F2-IsoPs maintained the positive associations with IFN-γ, TNF-α, and IL-2.
Conclusion: We did not find any specific blood biomarkers that could differentiate COPD patients with prevalent airway disease from those with prevalent emphysema. The MCP-1 increase in COPD-E, associated with the imbalance of oxidant/antioxidant markers, may play a role in inducing emphysema.
Keywords: serum, phenotypes, endotypes, biomarkers, asthma, airway inflammation
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