***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Background Because chronic obstructive pulmonary disease ( COPD ) is a heterogeneous condition , the identification of specific clinical phenotypes is key to developing more effective therapies . To explore if the persistence of systemic inflammation is associated with poor clinical outcomes in COPD we assessed patients recruited to the well-characterized ECLIPSE cohort ( NCT00292552 ) . Methods and Findings Six inflammatory biomarkers in peripheral blood ( white blood cells ( WBC ) count and CRP , IL-6 , IL-8 , fibrinogen and TNF-α levels ) were quantified in 1,755 COPD patients , 297 smokers with normal spirometry and 202 non-smoker controls that were followed-up for three years . We found that , at baseline , 30 % of COPD patients did not show evidence of systemic inflammation whereas 16 % had persistent systemic inflammation . Even though pulmonary abnormalities were similar in these two groups , persistently inflamed patients during follow-up had significantly increased all-cause mortality ( 13 % vs. 2 % , p<0.001 ) and exacerbation frequency ( 1.5 ( 1.5 ) vs. 0.9 ( 1.1 ) per year , p<0.001 ) compared to non-inflamed ones . As a descriptive study our results show associations but do not prove causality . Besides this , the inflammatory response is complex and we studied only a limited panel of biomarkers , albeit they are those investigated by the majority of previous studies and are often and easily measured in clinical practice . Conclusions Overall , these results identify a novel systemic inflammatory COPD phenotype that may be the target of specific research and treatment BACKGROUND Low- grade systemic inflammation is common in chronic obstructive pulmonary disease ( COPD ) , but its source remains unclear . Adipose tissue is a potent producer of inflammatory mediators and may contribute to systemic inflammation in COPD , possibly via hypoxia . OBJECTIVE We studied the influence of COPD and exercise-induced oxygen desaturation on adipose tissue inflammation ( ATI ) and its contribution to systemic inflammation . DESIGN Subcutaneous adipose tissue biopsies were investigated in 28 clinical ly stable COPD patients [ forced expiratory volume in 1 s : 58 ± 16 % predicted ; BMI ( in kg/m(2 ) ) : 24.9 ± 2.9 ] and 15 age- , sex- , and body composition-matched healthy control subjects . Fat mass was measured with dual-energy X-ray absorptiometry . Patients were prestratified by oxygen desaturation assessed by incremental cycle ergometry . The adipocyte size and adipose tissue expression of 19 inflammatory and hypoxia-related genes were measured , and adipose tissue macrophages ( ATMs ) were histologically quantified . Systemic inflammatory markers included C-reactive protein ( CRP ) and a panel of 20 adipokines . RESULTS COPD patients had comparable fat mass but higher CRP and HOMA-IR than did control subjects . COPD patients and control subjects had comparable adipose tissue gene expression , adipocyte size , ATM infiltration , and systemic adipokine concentrations . Desaturating COPD patients had no different ATI status than did nondesaturating COPD patients . COPD patients with high CRP had significantly greater ATM infiltration than did patients with low CRP , which was independent of BMI and fat mass . CONCLUSIONS In COPD patients , mild-to-moderate COPD , per se , does not enhance ATI or its contribution to systemic inflammation compared with in well-matched healthy control subjects . However , to our knowledge , our study provides a first indication for a possible role of ATMs in the systemic inflammatory response in COPD that requires additional investigation . This trial was registered at www.trialregister.nl as NTR1402 Chronic obstructive pulmonary disease ( COPD ) is associated with increased whole body protein breakdown and low- grade systemic inflammation . We aim ed to determine if physical training of patients with COPD induces anti-inflammatory effects and decreases whole-body protein breakdown .  Nineteen subjects with severe ( FEV(1)=31+/-1 ) COPD were r and omized into a training group ( n=9 ) and a control group ( n=10 ) . Twenty healthy subjects were studied for baseline comparison . The " COPD training " group participated in an outpatient rehabilitation program consisting of endurance training ( walking at 85 % of VO(2max ) ) twice weekly for 7 weeks plus daily home-based training .  Maximum walking distance increased by almost 70 % in the training group after 7 weeks of training . At baseline , the concentrations of C-reactive protein ( CRP ) and IL-18 in plasma were increased in subjects with COPD compared with healthy subjects ( P<0.05 ) and leucine rate of appearance ( R(a ) ) was approximately 15 % greater ( P<0.05 ) in subjects with COPD . Training had no effect on the plasma concentration of inflammatory markers but decreased leucine R(a ) in subjects with COPD by approximately 10 % ( P<0.05 ) . In conclusion , 7 weeks of physical training markedly improved endurance in patients with COPD and accelerated whole-body protein breakdown in patients with COPD was attenuated by physical training independent of changes in inflammatory markers Despite a number of studies on biomarkers in chronic obstructive pulmonary disease ( COPD ) , only a few disease-related markers have been identified , yet we still have no satisfactory markers specific to innate immune system and neutrophil activation , which is essential in airway inflammation in COPD . Recent biological studies indicated that lipocalins ( LCNs ) might be involved in airway inflammation and innate immunity ; however , results from available studies on the association of LCNs with COPD are not consistent . We carried out a multicenter prospect i ve observational cohort study to investigate the differences in serum levels  of LCN1 and LCN2 between subjects with COPD ( n=58 ) and healthy controls ( n=29 ) . Several vali date d inflammatory markers , including C-reactive protein , tumor necrosis factor-α , interleukin-6 , and interleukin-8 , were measured . The correlation of LCN1 and LCN2 with clinical features such as smoking habits , lung function , symptoms , and disease category was also analyzed . When comparing with healthy controls , serum levels of LCN1 ( 66.35±20.26 ng/mL versus 41.16±24.19 ng/mL , P<0.001 ) and LCN2 ( 11.29±3.92 ng/mL versus 6.09±5.13 ng/mL , P<0.001 ) were both elevated in subjects with COPD after adjusting for age , sex , smoking habits , and inflammatory biomarkers . Smoking history and tobacco exposure , as quantified by pack-year , had no impact on systemic expressions of LCN1 and LCN2 in our study . Blood levels of LCN1 and LCN2 , respectively , were negatively correlated to COPD Assessment Test and Modified Medical British Research Council score ( P<0.001 ) . Disease category by Global Initiative for Chronic Obstructive Lung Disease grade 1–4 or group A – D was not associated with levels of LCNs . Patient-reported exacerbations and body mass index were also tested , but no relationship with LCNs was found . In summary , serum concentrations of LCN1 and LCN2 were both elevated in patients with COPD , with their levels correlating to COPD Assessment Test and Modified Medical British Research Council score . These findings warrant large-scale and longitudinal studies to vali date LCNs as circulating biomarkers for COPD The aim of this study was to assess the expression levels of induced sputum interleukin (IL)-8 and IL-10 levels in patients with acute exacerbated chronic obstructive pulmonary disease ( AE COPD ) complicated with chronic cor pulmonale ( CCP ) at high altitude , and to evaluate the intervention effects of an inhaled corticosteroid ( ICS ) and a β2-adrenoceptor agonist in this disease . A total of 186 patients with AE COPD complicated with CCP were r and omly divided into three groups , with 62 cases in each . With regard to the two treatment groups , group A was treated with salmeterol/fluticasone ( 50 μg/250 μg , respectively ) by airway inhalation twice daily , while group B received budesonide ( 1 mg ) as a spray inhalation , twice daily . The routine treatment group ( group C ) received only routine treatment . The levels of IL-8 and IL-10 in the induced sputum and the predicted percentage of forced expiratory volume in one second ( FEV1%pred ) , partial pressure of oxygen in arterial blood ( PaO2 ) and partial pressure of carbon dioxide in arterial blood ( PaCO2 ) were examined on admission and at a stable stage two weeks following treatment . Forty healthy volunteers served as a control group ( group D ) . Compared with group D values , the IL-8 induced sputum level and the PaCO2 were significantly increased , while the level of IL-10 , FEV1%pred and the PaO2 were markedly decreased in the three COPD groups prior to treatment . Following treatment , the induced sputum IL-8 level and the PaCO2 were significantly decreased , while the induced sputum IL-10 level , FEV1%pred and the PaO2 were markedly increased in the three treatment groups compared with the values pre-therapy ( all P<0.01 ) . The post-treatment parameters were significantly different among the three groups ( P<0.01 ) . The results indicate that IL-8 and IL-10 are involved in the airway inflammation of AE COPD complicated by CCP . Treatment with an ICS was demonstrated to be a successful method of reducing the local expression of IL-8 and increasing the local expression of IL-10 ; however , ICS combined with a long-acting β2-adrenoceptor agonist ( LABA ) was more effective than the sole administration of ICS in patients with AE COPD complicated by CCP at high altitude In order to describe the outcomes of patients hospitalized with an acute exacerbation of severe chronic obstructive pulmonary disease ( COPD ) and determine the relationship between patient characteristics and length of survival , we studied a prospect i ve cohort of 1,016 adult patients from five hospitals who were admitted with an exacerbation of COPD and a PaCO2 of 50 mm Hg or more . Patient characteristics and acute physiology were determined . Outcomes were evaluated over a 6 mo period . Although only 11 % of the patients died during the index hospital stay , the 60-d , 180-d , 1-yr , and 2-yr mortality was high ( 20 % , 33 % , 43 % , and 49 % , respectively ) . The median cost of the index hospital stay was $ 7,100 ( $ 4,100 to $ 16,000 ; interquartile range ) . The median length of the index hospital stay was 9 d ( 5 to 15 d ) . After discharge , 446 patients were readmitted 754 times in the next 6 mo . At 6 mo , only 26 % of the cohort were both alive and able to report a good , very good , or excellent quality of life . Survival time was independently related to severity of illness , body mass index ( BMI ) , age , prior functional status , PaO2/FI(O2 ) , congestive heart failure , serum albumin , and the presence of cor pulmonale . Patients and caregivers should be aware of the likelihood of poor outcomes following hospitalization for exacerbation of COPD associated with hypercarbia BACKGROUND Chronic obstructive pulmonary disease ( COPD ) is characterised by chronic inflammation of the respiratory tract . METHODS We investigated the presence of interleukin-6 ( IL-6 : a cytokine secreted by monocytes/macrophages , T cells , B cells , fibroblasts , bone marrow stromal cells , keratinocytes and endothelial cells ) in the exhaled breath condensate of 16 exsmokers with moderate COPD , 12 healthy non-smokers .  IL-6 was measured by means of a specific enzyme immunoassay . RESULTS IL-6 levels were detectable in all of the subjects , but were higher in the COPD patients ( 8.0 + /- 0.1 pg/ml ; P < 0.0001 ) than in the healthy non-smokers ( 4.9 + /- 0.2 pg/ml ) with a correlation in this group between age and IL-6 levels ( r = 0.597 ; P < 0.05 ) . CONCLUSIONS The increased IL-6 levels in exhaled breath condensate may reflect airway inflammation in patients with COPD Chronic obstructive pulmonary disease ( COPD ) is characterized by an airway and systemic inflammatory response . Bioaerosols/organic dusts are important agricultural pollutants that may lead to COPD . These environments are complex , containing a rich source of various microbial components . The objective of this study was to determine whether individuals with COPD have enhanced systemic responsiveness to settled swine facility organic dust extract ( ODE ) or its main pathogenic components ( peptidoglycan [ PGN ] , lipopolysaccharide [ LPS ] ) versus healthy volunteers . A modified whole blood assay ( WBA ) that included occupational levels of ODE and concentrations of LPS and PGN found in ODE was used to determine systemic responsiveness ( mediator release ) , and sputum infl 
    Output:
    
Our findings suggested that COPD was associated with elevated serum CRP , leukocytes , IL-6 , IL-8 , and fibrinogen , without any significant relationship with TNF-α