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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

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      Differences in systemic inflammation between cigarette and biomass smoke-induced COPD

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          Abstract

          Background and objective

          It is known that biomarkers of systemic inflammation are raised in COPD caused by tobacco (T-COPD) compared with healthy controls, but there is less information on the inflammatory status of subjects with COPD caused by biomass smoke (B-COPD). In addition, the possible (if any) differences in inflammation between both types of the disease are still not well known. The aim of this study was to assess the inflammatory profile in B-COPD and T-COPD.

          Methods

          A total of 20 subjects (15 men and five women) with T-COPD were matched one to one for sex, age and forced expiratory volume in 1 s (FEV 1) to 20 B-COPD patients. In all, 20 sex-matched healthy subjects with normal lung function without smoking history or biomass exposure were included as controls. The following biomarkers were measured: exhaled nitric oxide, serum IL-6, IL-8, IL-5, IL-13, periostin, surfactant protein-P, TNF-α, IgE, erythrocyte sedimentation rate, C-reactive protein and fibrinogen. Complete blood count was also obtained.

          Results

          The age of the subjects was 70.2±7.9 years and FEV 1% was 56.2%±14.6%. Most inflammatory biomarkers were higher in both types of COPD than in healthy controls. IL-6, IL-8 and IL-5 were significantly higher in T-COPD than in B-COPD, without other significant differences.

          Conclusion

          Both types of COPD are associated with high levels of systemic inflammation biomarkers. T-COPD patients have a higher systemic inflammatory status than the patients with B-COPD.

          Most cited references27

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          An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease.

          Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.
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            Innate and adaptive immune responses in asthma.

            The recognition that asthma is primarily an inflammatory disorder of the airways associated with T helper type 2 (T(H)2) cell-dependent promotion of IgE production and recruitment of mast cells and eosinophils has provided the rationale for disease control using inhaled corticosteroids and other anti-inflammatory drugs. As more has been discovered about the cytokine, chemokine and inflammatory pathways that are associated with T(H)2-driven adaptive immunity, attempts have been made to selectively inhibit these in the hope of discovering new therapeutics as predicted from animal models of allergic inflammation. The limited success of this approach, together with the recognition that asthma is more than allergic inflammation, has drawn attention to the innate immune response in this disease. Recent advances in our understanding of the sentinel role played by innate immunity provides new targets for disease prevention and treatment. These include pathways of innate stimulation by environmental or endogenous pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DCs, innate sources of cytokines, and the identification of new T cell subsets and lymphoid cells.
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              From COPD to chronic systemic inflammatory syndrome?

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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
                01 September 2017
                : 12
                : 2639-2646
                Affiliations
                [1 ]Respiratory Medicine Service
                [2 ]Cardiology Service, University Hospital Lucus Augusti, Lugo
                [3 ]Medical-Surgical Unit of Respiratory Diseases, University Hospital Virgen del Rocío, Sevilla
                [4 ]Center for Biomedical Research in Respiratory Diseases Network, Carlos III Health Institute, Madrid, Spain
                Author notes
                Correspondence: Rafael Golpe, Servicio de Neumología, Hospital Universitario Lucus Augusti, Unidad Administrativa 4-A, c/Dr Ulises Romero, 1, 27002 Lugo, Spain, Tel +34 982 29 6859, Email rafael.golpe.gomez@ 123456sergas.es
                Article
                copd-12-2639
                10.2147/COPD.S141068
                5589102
                28979110
                6f65908e-e356-4ace-99c3-88add75dc6d0
                © 2017 Golpe 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.

                History
                Categories
                Original Research

                Respiratory medicine
                biomass smoke,copd,cytokines,inflammation,smoking
                Respiratory medicine
                biomass smoke, copd, cytokines, inflammation, smoking

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