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      Association between serum interleukin-6 concentrations and chronic obstructive pulmonary disease: a systematic review and meta-analysis

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          Abstract

          Background. Interleukin-6 (IL-6) is an important pro-inflammatory cytokine and has been implicated to play a role in the systemic inflammation of patients with chronic obstructive pulmonary disease (COPD). We conducted this meta-analysis to assess the association between serum IL-6 concentrations and COPD.

          Methods. PubMed and Embase were searched for eligible studies. Data were extracted by two investigators (Wei J, Xiong XF) independently and analyzed using Review Manager 5.3 and STATA 12.0 software. Standard mean differences (SMDs) and 95% confidence intervals (CI) were calculated.

          Results. Thirty-three studies were included in this meta-analysis. The serum IL-6 concentrations were higher in patients with stable COPD than healthy controls (SMD = 0.65, 95% CI [0.51–0.79]). COPD patients without major comorbidities also showed higher IL-6 levels than healthy controls (SMD = 0.74, 95% CI [0.56–0.91]). COPD patients with an forced expiratory volume in one second (FEV 1) of either <50% predicted or >50% predicted had increased IL-6 concentrations compared to healthy controls (SMD = 0.77, 95% CI [0.48–1.05], SMD = 1.01, 95% CI [0.43–1.59], respectively). The serum IL-6 concentrations between mild-moderate and severe-very severe COPD patient groups were not found to be significant (SMD = −0.1, 95% CI [−0.65–0.44]).

          Conclusions. This meta-analysis indicated that patients with stable COPD had higher serum IL-6 concentrations than healthy controls. No evidence showing positive or negative association between IL-6 concentrations and the severity of pulmonary function impairment was found. The correlation between IL-6 levels and pulmonary function was weak in different severities of stable COPD patients.

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          Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis.

          Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV(1)) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-alpha (TNF-alpha), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-alpha levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.
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            Chronic obstructive pulmonary disease: molecular and cellular mechanisms.

            Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective. There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases. The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.
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              Atherosclerosis is an inflammatory disease

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                Author and article information

                Contributors
                Journal
                PeerJ
                PeerJ
                PeerJ
                PeerJ
                PeerJ
                PeerJ Inc. (San Francisco, USA )
                2167-8359
                27 August 2015
                2015
                : 3
                : e1199
                Affiliations
                [1 ]Department of Respiratory Medicine, West China Hospital of Sichuan University , Chengdu, Sichuan, China
                [2 ]Department of Respiratory Medicine, First Affiliated Hospital of Xiamen University , Xiamen, Fujian, China
                [3 ]Department of Respiratory Medicine, Third People’s Hospital , Chengdu, Sichuan, China
                Article
                1199
                10.7717/peerj.1199
                4556145
                26336642
                dd0de649-03b1-4fab-9a69-c89a47067d2f
                © 2015 Wei et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.

                History
                : 5 June 2015
                : 29 July 2015
                Funding
                The authors received no funding for this work.
                Categories
                Respiratory Medicine

                meta-analysis,chronic obstructive pulmonary disease,systemic inflammation,interleukin-6,pulmonary function

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