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      Correlation of serum levels of HIF-1α and IL-19 with the disease progression of COPD: a retrospective study

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          Abstract

          Background

          The aim of this study was to disclose the correlation between the serum levels of hypoxia-inducible factor 1 alpha (HIF-1α) and IL-19 and stable COPD.

          Methods

          The serum levels of HIF-1α and IL-19 were tested by ELISA. The relationships between their levels and clinical parameters of stable COPD patients were analyzed by linear regression methods.

          Results

          Patients with stable COPD showed higher serum levels of HIF-1α and IL-19 compared with healthy control group ( P<0.001), and serum levels of HIF-1α and IL-19 had a positive linear correlation ( P<0.05). In stable COPD patients, increased serum levels of HIF-1α and IL-19 were positively correlated with the GOLD grading ( P<0.005), modified British Medical Research Council (mMRC) score ( P<0.05), and medical history ( P<0.05) but negatively related to the pulmonary function ( P<0.05). The serum level of HIF-1α ( P<0.05) was affected by the patient’s FEV 1/FVC value and COPD grading, and the serum level of IL-19 was associated with the mMRC scores and the serum level of HIF-1α ( P<0.05).

          Conclusion

          Increased serum levels of HIF-1α and IL-19 correlated with the disease progression of COPD, suggesting that they can be used as indicators to help us understand the COPD.

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          Most cited references 24

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          Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Lung Disease 2017 Report: GOLD Executive Summary.

          This Executive Summary of the Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 Report focuses primarily on the revised and novel parts of the document. The most significant changes include: (i) the assessment of chronic obstructive pulmonary disease has been refined to separate the spirometric assessment from symptom evaluation. ABCD groups are now proposed to be derived exclusively from patient symptoms and their history of exacerbations; (ii) for each of the groups A to D, escalation strategies for pharmacological treatments are proposed; (iii) the concept of de-escalation of therapy is introduced in the treatment assessment scheme; (iv)non-pharmacological therapies are comprehensively presented and (v) the importance of co-morbid conditions in managing COPD is reviewed.
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            Cellular and molecular mechanisms of asthma and COPD.

             Peter Barnes (2017)
            Asthma and chronic obstructive pulmonary disease (COPD) both cause airway obstruction and are associated with chronic inflammation of the airways. However, the nature and sites of the inflammation differ between these diseases, resulting in different pathology, clinical manifestations and response to therapy. In this review, the inflammatory and cellular mechanisms of asthma and COPD are compared and the differences in inflammatory cells and profile of inflammatory mediators are highlighted. These differences account for the differences in clinical manifestations of asthma and COPD and their response to therapy. Although asthma and COPD are usually distinct, there are some patients who show an overlap of features, which may be explained by the coincidence of two common diseases or distinct phenotypes of each disease. It is important to better understand the underlying cellular and molecular mechanisms of asthma and COPD in order to develop new treatments in areas of unmet need, such as severe asthma, curative therapy for asthma and effective anti-inflammatory treatments for COPD.
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              Cytokine inhibition in the treatment of COPD

              Cytokines play an important part in many pathobiological processes of chronic obstructive pulmonary disease (COPD), including the chronic inflammatory process, emphysema, and altered innate immune response. Proinflammatory cytokines of potential importance include tumor necrosis factor (TNF)-α, interferon-γ, interleukin (IL)-1β, IL-6, IL-17, IL-18, IL-32, and thymic stromal lymphopoietin (TSLP), and growth factors such as transforming growth factor-β. The current objectives of COPD treatment are to reduce symptoms, and to prevent and reduce the number of exacerbations. While current treatments achieve these goals to a certain extent, preventing the decline in lung function is not currently achievable. In addition, reversal of corticosteroid insensitivity and control of the fibrotic process while reducing the emphysematous process could also be controlled by specific cytokines. The abnormal pathobiological process of COPD may contribute to these fundamental characteristics of COPD, and therefore targeting cytokines involved may be a fruitful endeavor. Although there has been much work that has implicated various cytokines as potentially playing an important role in COPD, there have been very few studies that have examined the effect of specific cytokine blockade in COPD. The two largest studies that have been reported in the literature involve the use of blocking antibody to TNFα and CXCL8 (IL-8), and neither has provided benefit. Blocking the actions of CXCL8 through its CXCR2 receptor blockade was not successful either. Studies of antibodies against IL-17, IL-18, IL-1β, and TSLP are currently either being undertaken or planned. There is a need to carefully phenotype COPD and discover good biomarkers of drug efficacy for each specific target. Specific groups of COPD patients should be targeted with specific anticytokine therapy if there is evidence of high expression of that cytokine and there are features of the clinical expression of COPD that will respond.
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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
                2018
                21 November 2018
                : 13
                : 3791-3803
                Affiliations
                [1 ]Department of Respiratory Medicine, First Affiliated Hospital, Xi’an Medical University, Xi’an, China, research568rbx@ 123456yeah.net
                [2 ]Comprehensive Medicine Department, Shenmu Hospital, Shenmu, China
                [3 ]Department of Respiratory Medicine, Shenmu Hospital, Shenmu, China
                [4 ]Department of Respiratory Medicine, Jining No 1 People’s Hospital, Jining, China
                [5 ]Institute of Epidemiology and Health Statistics, School of Public Health, Lanzhou University, Lanzhou, China
                [6 ]Department of Respiratory Medicine, Gansu Provincial Hospital, Lanzhou, China
                Author notes
                Correspondence: Biaoxue Rong, Department of Respiratory Medicine, First Affiliated Hospital, Xi’an Medical University, 48 Fenghao West Road, Xi’an 710077, China, Tel +86 29 8767 9300, Email research568rbx@ 123456yeah.net
                Article
                copd-13-3791
                10.2147/COPD.S177034
                6254505
                © 2018 Rong 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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