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      Predictive Value of Serum Markers SFRP1 and CC16 in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

      research-article
      Author(s): , , ,
      Publication date (Electronic):
      Journal: Evidence-based Complementary and Alternative Medicine : eCAM
      Publisher: Hindawi

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          Abstract

          Background

          Chronic obstructive pulmonary disease (COPD) patients are particularly vulnerable to acute exacerbation, resulting in a huge socioeconomic burden.

          Objective

          In this study, we evaluated the value of serum secreted frizzled-related protein 1 (SFRP1) and Clara cell-secreted protein (CC16) in predicting the risk of acute exacerbations in patients with COPD.

          Methods

          The study included 123 COPD patients admitted to our hospital from May 2020 to June 2021, including 65 patients in stable stage (STCOPD group), 58 patients in acute exacerbation stage (AECOPD group), and 60 healthy volunteers (control group). Serum SFRP1 and CC16 levels were detected by enzyme-linked immunosorbent assay (ELISA). The receiver operating characteristics curve (ROC) analysis was performed to evaluate the sensitivity and specificity of serum SFRP1 and CC16 for predicting the risk of acute exacerbation in COPD patients.

          Results

          The age among groups is significantly different, but there is no difference in the gender and body mass index (BMI). The level of serum SFRP1 in the AECOPD group was significantly higher than that in the STCOPD group and the control group, and the level of serum CC16 was lower than that in the STCOPD group and the control group. Serum SFRP1 was negatively correlated with forced expiratory volume in one second (FEV 1)/forced vital capacity (FVC) ( r = −0.473, P < 0.001). Serum CC16 was positively correlated with FEV 1/FVC ( r = 0.457, P < 0.001). The area under the curve (AUC), sensitivity, and specificity of SFRP1 for predicting the risk of exacerbation was 0.847 (95% CI: 0.775 to 0.920), 86.20%, and 80.00%. The AUC, sensitivity, and specificity of CC16 for predicting the risk of exacerbation were 0.795 (95% CI: 0.711 to 0.879), 74.10%, and 86.20%.

          Conclusions

          These findings suggest that SFRP1 and CC16 may be useful serum markers for predicting the risk of exacerbation in COPD patients.

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          Most cited references24

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          Wnt/beta-catenin signaling: components, mechanisms, and diseases.

          Bryan T MacDonald, Keiko Tamai, Xi. He (2009)
          Signaling by the Wnt family of secreted glycolipoproteins via the transcriptional coactivator beta-catenin controls embryonic development and adult homeostasis. Here we review recent progress in this so-called canonical Wnt signaling pathway. We discuss Wnt ligands, agonists, and antagonists, and their interactions with Wnt receptors. We also dissect critical events that regulate beta-catenin stability, from Wnt receptors to the cytoplasmic beta-catenin destruction complex, and nuclear machinery that mediates beta-catenin-dependent transcription. Finally, we highlight some key aspects of Wnt/beta-catenin signaling in human diseases including congenital malformations, cancer, and osteoporosis, and discuss potential therapeutic implications.
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            Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2017 Report. GOLD Executive Summary

            Claus F. Vogelmeier, Gerard J. Criner, Fernando J Martínez … (2017)
            American Journal of Respiratory and Critical Care Medicine, 195(5), 557-582
            Article 0 comments Cited 736 times – based on 0 reviews     Review now
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              Inflammatory mechanisms in patients with chronic obstructive pulmonary disease.

              Peter Barnes (2016)
              Chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation affecting predominantly the lung parenchyma and peripheral airways that results in largely irreversible and progressive airflow limitation. This inflammation is characterized by increased numbers of alveolar macrophages, neutrophils, T lymphocytes (predominantly TC1, TH1, and TH17 cells), and innate lymphoid cells recruited from the circulation. These cells and structural cells, including epithelial and endothelial cells and fibroblasts, secrete a variety of proinflammatory mediators, including cytokines, chemokines, growth factors, and lipid mediators. Although most patients with COPD have a predominantly neutrophilic inflammation, some have an increase in eosinophil counts, which might be orchestrated by TH2 cells and type 2 innate lymphoid cells though release of IL-33 from epithelial cells. These patients might be more responsive to corticosteroids and bronchodilators. Oxidative stress plays a key role in driving COPD-related inflammation, even in ex-smokers, and might result in activation of the proinflammatory transcription factor nuclear factor κB (NF-κB), impaired antiprotease defenses, DNA damage, cellular senescence, autoantibody generation, and corticosteroid resistance though inactivation of histone deacetylase 2. Systemic inflammation is also found in patients with COPD and can worsen comorbidities, such as cardiovascular diseases, diabetes, and osteoporosis. Accelerated aging in the lungs of patients with COPD can also generate inflammatory protein release from senescent cells in the lung. In the future, it will be important to recognize phenotypes of patients with optimal responses to more specific therapies, and development of biomarkers that identify the therapeutic phenotypes will be important.
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                Author and article information

                Contributors
                Junlan Gao:
                ORCID: https://orcid.org/0000-0001-5822-2464
                Journal
                Journal ID (nlm-ta): Evid Based Complement Alternat Med
                Journal ID (iso-abbrev): Evid Based Complement Alternat Med
                Journal ID (publisher-id): ECAM
                Title: Evidence-based Complementary and Alternative Medicine : eCAM
                Publisher: Hindawi
                ISSN (Print): 1741-427X
                ISSN (Electronic): 1741-4288
                Publication date Collection: 2022
                Publication date (Electronic): 2 August 2022
                Publication date PMC-release: 2 August 2022
                Volume: 2022
                Electronic Location Identifier: 6488935
                Affiliations
                Department of Critical Care Medicine, Second Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
                Author notes

                Academic Editor: Bo Li

                Author information
                https://orcid.org/0000-0001-9194-3706
                https://orcid.org/0000-0001-5822-2464
                Article
                DOI: 10.1155/2022/6488935
                PMC ID: 9363185
                PubMed ID: 35958937
                SO-VID: e3c5e8fd-988f-4c72-b8ca-e9a8fedd81f0
                Copyright © Copyright © 2022 Yewei He et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 14 June 2022
                Date revision received : 10 July 2022
                Date accepted : 12 July 2022
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Complementary & Alternative medicine
                Data availability:
                ScienceOpen disciplines: Complementary & Alternative medicine

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