scholarly journals Emphysema and extrapulmonary tissue loss in COPD: a multi-organ loss of tissue phenotype

2018 ◽  
Vol 51 (2) ◽  
pp. 1702146 ◽  
Author(s):  
Bartolome R. Celli ◽  
Nicholas Locantore ◽  
Ruth Tal-Singer ◽  
John Riley ◽  
Bruce Miller ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Forced Expiratory Volume ◽  
Fat Free Mass ◽  
Tissue Loss ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Club Cell ◽  
Body Compartments

We tested whether emphysema progression accompanies enhanced tissue loss in other body compartments in 1817 patients from the ECLIPSE chronic obstructive pulmonary disease (COPD) cohort.Clinical and selected systemic biomarker measurements were compared in subjects grouped by quantitative tomography scan emphysema quartiles using the percentage of low attenuation area (LAA%). Lowest and highest quartile patients had amino-acid metabolomic profiles. We related LAA% to 3 years decline in lung function (forced expiratory volume in 1 s (FEV1)), body mass index (BMI), fat-free mass index (FFMI) and exacerbations, hospitalisations and mortality rates.Participants with more baseline emphysema had lower FEV1, BMI and FFMI, worse functional capacity, and less cardiovascular disease but more osteoporosis. Systemic C-reactive protein and interleukin-6 levels were similar among groups, but club cell protein 16 was higher and interleukin-8, surfactant protein D and soluble receptor for advanced glycation end product were lower with more emphysema. Metabolomics differed between extreme emphysema quartiles. Patients with more emphysema had accelerated FEV1, BMI and FFMI decline and more exacerbations, hospitalisations and mortality.COPD patients with more emphysema undergo excessive loss of pulmonary and extrapulmonary tissue, which is probably related to abnormal tissue maintenance. Because of worse clinical outcomes, we propose this subgroup be named the multi-organ loss of tissue (MOLT) COPD phenotype.

scholarly journals Serum biomarkers and outcomes in patients with moderate COPD: a substudy of the randomised SUMMIT trial

2019 ◽  
Vol 6 (1) ◽  
pp. e000431 ◽  
Author(s):  
Bartolome R Celli ◽  
Julie A Anderson ◽  
Robert Brook ◽  
Peter Calverley ◽  
Nicholas J Cowans ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Forced Expiratory Volume ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Mortality And Morbidity ◽  
Copd Exacerbations ◽  
Club Cell ◽  
Risk Of Death ◽  
Increased Risk

RationaleSystemic levels of C reactive protein (CRP), surfactant protein D (SPD), fibrinogen, soluble receptor of activated glycogen end-product (sRAGE) and club cell protein 16 (CC-16) have been associated with chronic obstructive pulmonary disease (COPD) outcomes. However, they require validation in different cohorts.ObjectivesRelate systemic levels of those proteins to forced expiratory volume in 1 s (FEV1) decline, exacerbations, hospitalisations and mortality in COPD patients (FEV1 of ≥50 and ≤70% predicted) and heightened cardiovascular risk in a substudy of the Study to Understand Mortality and MorbidITy trial.MethodsParticipants were randomised to daily inhalations of placebo, vilanterol 25 µg (VI), fluticasone furoate 100 µg (FF) or their combination (VI 25/FF 100) and followed quarterly until 1000 deaths in the overall 16 485 participants occurred. Biomarker blood samples were available from 1673 patients. The FEV1 decline (mL/year), COPD exacerbations, hospitalisations and death were determined. Associations between biomarker levels and outcomes were adjusted by age and gender.ResultsSystemic levels of CC-16, CRP, sRAGE, SPD and fibrinogen did not relate to baseline FEV1, FEV1 decline, exacerbations or hospitalisations. Fibrinogen and CRP were related to mortality over a median follow-up of 2.3 years. Only the CC-16 changed with study therapy (VI, FF and FF/VI, p<0.01) at 3 months.ConclusionsIn COPD, systemic levels of CC-16, CRP, sRAGE, SPD and fibrinogen were not associated with FEV1 decline, exacerbations or hospitalisations. These results cast doubts about the clinical usefulness of the systemic levels of these proteins as surrogate markers of these COPD outcomes. The study confirms that CRP and fibrinogen are associated with increased risk of death in patients with COPD.Trial registration numberNCT01313676.

scholarly journals Biomarkers in Airway Diseases

2013 ◽  
Vol 20 (3) ◽  
pp. 180-182 ◽  
Author(s):  
Janice M Leung ◽  
Don D Sin
Keyword(s):  
Clinical History ◽  
Surfactant Protein ◽  
Secretory Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Club Cell ◽  
Disease Phenotypes ◽  
Airway Diseases ◽  
Steroid Responsiveness

The inherent limitations of spirometry and clinical history have prompted clinicians and scientists to search for surrogate markers of airway diseases. Although few biomarkers have been widely accepted into the clinical armamentarium, the authors explore three sources of biomarkers that have shown promise as indicators of disease severity and treatment response. In asthma, exhaled nitric oxide measurements can predict steroid responsiveness and sputum eosinophil counts have been used to titrate anti-inflammatory therapies. In chronic obstructive pulmonary disease, inflammatory plasma biomarkers, such as fibrinogen, club cell secretory protein-16 and surfactant protein D, can denote greater severity and predict the risk of exacerbations. While the multitude of disease phenotypes in respiratory medicine make biomarker development especially challenging, these three may soon play key roles in the diagnosis and management of airway diseases.

scholarly journals Pneumoproteins in Offshore Drill Floor Workers

2019 ◽  
Vol 16 (3) ◽  
pp. 300 ◽  
Author(s):  
Niels E. Kirkhus ◽  
Bente Ulvestad ◽  
Lars Barregard ◽  
Øivind Skare ◽  
Raymond Olsen ◽  
...  
Keyword(s):  
Strong Association ◽  
Surfactant Protein ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Drilling Mud ◽  
Air Concentration ◽  
Work Period ◽  
Club Cell ◽  
Before And After ◽  
Oil Mist

The aim was to assess pneumoproteins and a certain biomarker of systemic inflammation in drill floor workers exposed to airborne contaminants generated during drilling offshore, taking into consideration serum biomarkers of smoking, such as nicotine (S-Nico) and cotinine. Blood samples of club cell protein 16 (CC-16), surfactant protein D (SP-D) and C-reactive protein (CRP) were collected before and after a 14-day work period from 65 drill floor workers and 65 referents. Air samples of oil mist, drilling mud components and elemental carbon were collected in person. The drill floor workers were exposed to a median air concentration of 0.18 mg/m3 of oil mist and 0.14 mg/m3 of airborne mud particles. There were no differences in the concentrations of CC-16 and SP-D across the 14-day work period and no difference between drill floor workers and referents at baseline after adjusting for differences in sampling time and smoking. CRP decreased across the work period. There was a strong association between the CC-16 concentrations and the time of sampling. Current smokers with S-Nico > detection limit (DL) had a statistically significantly lower CC-16 concentration, while smokers with S-Nico <DL had CC-16 concentrations similar to that of the non-smokers. Fourteen days of work offshore had no effect on serum pneumoprotein and CRP concentrations. However, the time of blood sampling was observed to have a strong effect on the measured concentrations of CC-16. The effect of current smoking on the CC-16 concentrations appears to be dependent on the S-Nico concentrations.

Particle depletion of diesel exhaust restores allergen-induced lung-protective surfactant protein D in human lungs

Thorax ◽  
2020 ◽  
Vol 75 (8) ◽  
pp. 640-647 ◽  
Author(s):  
Min Hyung Ryu ◽  
Kevin Soon-Keen Lau ◽  
Denise Jill Wooding ◽  
Shuyu Fan ◽  
Don D Sin ◽  
...  
Keyword(s):  
Air Pollution ◽  
Diesel Exhaust ◽  
Surfactant Protein ◽  
Systemic Circulation ◽  
Regulatory Proteins ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Asthma Morbidity ◽  
Club Cell ◽  
Human Airways

RationaleExposure to air pollution is linked with increased asthma morbidity and mortality. To understand pathological processes linking air pollution and allergen exposures to asthma pathophysiology, we investigated the effect of coexposure to diesel exhaust (DE) and aeroallergen on immune regulatory proteins in human airways.MethodsFourteen allergen-sensitised participants completed this randomised, double-blinded, cross-over, controlled exposure study. Each participant underwent four exposures (allergen-alone exposure, DE and allergen coexposure, particle-depleted DE (PDDE) and allergen coexposure, and sham exposure) on different order-randomised dates, each separated by a 4-week washout. Serum and bronchoalveolar lavage (BAL) were assayed for pattern recognition molecules, cytokines, chemokines and inflammatory mediators.ResultsIn human airways, allergen-alone exposure led to accumulation of surfactant protein D (SPD; p=0.02). Coexposure to allergen and DE did not elicit the same increase of SPD as did allergen alone; diesel particulate reduction restored allergen-induced SPD accumulation. Soluble receptor for advanced glycation end products was higher with particle reduction than without it. In the systemic circulation, there was a transient increase in SPD and club cell protein 16 (CC16) 4 hours after allergen alone. CC16 was augmented by PDDE, but not DE. % eosinophils in BAL (p<0.005), eotaxin-3 (p<0.0001), interleukin 5 (IL-5; p<0.0001) and thymus and activation regulated chemokine (p=0.0001) were each increased in BAL by allergen. IL-5, SPD and % eosinophils in BAL were correlated with decreased FEV1.ConclusionShort-term coexposure to aeroallergen and DE alters immune regulatory proteins in lungs; surfactant levels are dependent on particle depletion.Trial registration numberNCT02017431.

Surfactant protein D in chronic obstructive pulmonary disease and type 2 diabetes mellitus

2017 ◽  
Vol 30 (1) ◽  
pp. 297
Author(s):  
MaiA.H. Abou Elenin ◽  
NaglaaM Ghanayem ◽  
ElsayedS Abou Elnour ◽  
RababA El Wahsh ◽  
RaniaM.A. El-Shazlya
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Chronic Obstructive Pulmonary Disease ◽  
Type 2 Diabetes Mellitus ◽  
Pulmonary Disease ◽  
Surfactant Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease
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