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      Anti- p-benzoquinone antibody level as a prospective biomarker to identify smokers at risk for COPD

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          Abstract

          Background and objective

          Identification of smokers having predisposition to COPD is important for early intervention to reduce the huge global burden of the disease. Using a guinea pig model, we have shown that p-benzoquinone ( p-BQ) derived from cigarette smoke (CS) in the lung is a causative factor for CS-induced emphysema. p-BQ is also derived from CS in smokers and it elicits the production of anti- p-BQ antibody in humans. We therefore hypothesized that anti- p-BQ antibody might have a protective role against COPD and could be used as a predictive biomarker for COPD in smokers. The objective of this study was to compare the serum anti- p-BQ antibody level between smokers with and without COPD for the evaluation of the hypothesis.

          Methods

          Serum anti- p-BQ antibody concentrations of current male smokers with (n=227) or without (n=308) COPD were measured by an indirect enzyme-linked immunoabsorbent assay (ELISA) developed in our laboratory. COPD was diagnosed by spirometry according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines.

          Results and discussion

          A significant difference was observed in the serum anti- p-BQ antibody level between smokers with and without COPD (Mann–Whitney U-test =4,632.5, P=0.000). Receiver operating characteristic (ROC) curve analysis indicated that the ELISA had significant precision (area under the curve [AUC] =0.934, 95% confidence interval [CI]: 0.913–0.935) for identifying smokers with COPD from their low antibody level. The antibody cutoff value of 29.4 mg/dL was constructed from the ROC coordinates to estimate the risk for COPD in smokers. While 90.3% of smokers with COPD had a low antibody value (≤29.4 mg/dL), the majority (86.4%) of smokers without COPD had a high antibody value (≤29.4 mg/dL); 13.6% of current smokers without COPD having an antibody level below this cutoff value (odds ratio [OR] =59.3, 95% CI: 34.15–101.99) were considered to be at risk for COPD.

          Conclusion and future directions

          Our results indicate that serum anti- p-BQ antibody level may be used as a biomarker to identify asymptomatic smokers at risk for COPD for early intervention of the disease.

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          Most cited references 19

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          Oxidative stress in chronic obstructive pulmonary disease. Oxidative Stress Study Group.

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            Screening for and early detection of chronic obstructive pulmonary disease.

            Chronic obstructive pulmonary disease (COPD) is a substantially underdiagnosed disorder, with the diagnosis typically missed or delayed until the condition is advanced. Spirometry is the most frequently used pulmonary function test and enables health professionals to make an objective measurement of airflow obstruction and assess the degree to which it is reversible. As a diagnostic test for COPD, spirometry is a reliable, simple, non-invasive, safe, and non-expensive procedure. Early diagnosis of COPD should provide support for smoking cessation initiatives and lead to reduction of the societal burden of the disease, but definitive confirmation of both proves elusive. Despite substantial effort and investment, implementation of quality spirometry is deficient because of several hurdles and limitations, described in this Review. All in all, spirometry is recognised as the essential test for diagnosis and monitoring of COPD.
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              Pulmonary biomarkers in chronic obstructive pulmonary disease.

              There has been increasing interest in using pulmonary biomarkers to understand and monitor the inflammation in the respiratory tract of patients with chronic obstructive pulmonary disease (COPD). In this Pulmonary Perspective we discuss the merits of the various approaches by reviewing the current literature on pulmonary biomarkers in COPD and underscore the need for more systematic studies in the future. Bronchial biopsies and bronchoalveolar lavage provide valuable information about inflammatory cells and mediators, but are invasive, so that repeated measurements have to be very limited in assessing any interventions. Induced sputum has provided considerable information about the inflammatory process, including mediators and proteinases in COPD, but selectively samples proximal airways and may not closely reflect distal inflammatory processes. Exhaled gases and breath condensate are noninvasive procedures, so repeated measurements are possible, but for some assays the variability is relatively high. There is relatively little information about how any of these biomarkers relate to other clinical outcomes, such as progression of the disease, severity of disease, clinical subtypes, or response to therapy. More information is also needed about the variability in these measurements. In the future, pulmonary biomarkers may be useful in predicting disease progression, indicating disease instability, and in predicting response to current therapies and novel therapies, many of which are now in development.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2017
                21 June 2017
                : 12
                : 1847-1856
                Affiliations
                [1 ]Department of Biotechnology and Dr B C Guha Centre for Genetic Engineering and Biotechnology, University College of Science and Technology, University of Calcutta
                [2 ]Institute of Pulmocare and Research
                [3 ]Department of Pulmonary Medicine, Calcutta National Medical College
                [4 ]Department of Chest Medicine, Institute of Post Graduate Medical Education and Research
                [5 ]National Institute of Cholera and Enteric Diseases, Kolkata, India
                Author notes
                Correspondence: Indu B Chatterjee, Department of Biotechnology and Dr B C Guha Centre for Genetic Engineering and Biotechnology, University College of Science and Technology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, 700019, India, Tel +91 983 049 3842, Email ibchatterjee123@ 123456gmail.com
                Article
                copd-12-1847
                10.2147/COPD.S134455
                5485895
                © 2017 Banerjee et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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