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Tumor necrosis factor receptor 2 as a possible marker of COPD in smokers and ex-smokers

Authors Caram LMO, Ferrari R, Nogueira DL, Oliveira MRM, Francisqueti FV, Tanni SE, Corrêa CR, Godoy I

Received 1 April 2017

Accepted for publication 23 May 2017

Published 7 July 2017 Volume 2017:12 Pages 2015—2021

DOI https://doi.org/10.2147/COPD.S138558

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Charles Downs

Peer reviewer comments 2

Editor who approved publication: Dr Richard Russell

Laura Miranda de Oliveira Caram,1 R Ferrari,1 DL Nogueira,1 MRM Oliveira,2 FV Francisqueti,2 SE Tanni,1 CR Corrêa,2 I Godoy1

1Department of Internal Medicine, 2Department of Pathology, Botucatu Medical School, UNESP – Univ Estadual Paulista, Botucatu Campus, Botucatu-São Paulo, Brazil

Introduction: Oxidative stress and systemic inflammation are higher in smokers and patients with COPD; however, markers that may help differentiate between smokers and patients with COPD have not yet been identified. We hypothesized that tumor necrosis factor-alpha receptor (TNFR) and soluble form of the receptor for advanced glycation end products (sRAGE) can be indicators of COPD in asymptomatic patients.
Patients and methods: We evaluated 32 smokers (smoking history >10 pack-years), 32 patients with mild/moderate COPD (smokers and ex-smokers), and 32 never smokers. Concentrations of C-reactive protein (CRP), interleukin (IL)-6, TNFR1 and TNFR2, advanced glycation end products (AGEs), and the sRAGE were measured in serum.
Results: There were higher CRP and AGEs concentrations in smokers and in patients with COPD (P<0.001 and P=0.01, respectively) compared to controls, without statistical difference between smokers and patients with COPD. Concentrations of sRAGE, IL-6, and TNFR1 did not differ between study groups. TNFR2 was significantly higher in patients with COPD than in smokers (P=0.004) and controls (P=0.004), and the presence of COPD (P=0.02) and CRP (P=0.001) showed a positive association with TNFR2. Positive associations for smoking (P=0.04), CRP (P=0.03), and IL-6 (P=0.03) with AGEs were also found. The interaction variable (smoking × COPD) showed a positive association with IL-6.
Conclusion: Our data suggest that TNFR2 may be a possible marker of COPD in asymptomatic smokers and ex-smokers. Although smokers and patients with early COPD presented other increased systemic inflammation markers (eg, CRP) and oxidative stress (measured by AGEs), they did not differentiate smokers from COPD.

Keywords: smoking, chronic obstructive pulmonary disease, inflammation mediators, oxidative stress
 

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