The CIBERES Pulmonary Biobank Consortium: an opportunity for cooperative international respiratory research

Villena, Cristina; Pozo, Francisco del; Barberà, Joan Albert; Vaquer, Paloma; Agustí, Àlvar

doi:10.1183/09031936.00104210

Cited by 9 publications

(7 citation statements)

References 5 publications

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“…We studied lung tissue specimens (n=68) provided by the Pulmonary Biobank of CIBERES [ 14 ], which were obtained from patients undergoing lung resectional surgery because of localised lung cancer (n=54) or bilateral lung transplantation (n=14). 38 of them had COPD [ 2 ] (n=26, 71% on inhaled long-acting bronchodilators and corticosteroids), 15 were smokers (>10 pack-years) with normal spirometry and 15 were never-smokers ( table 1 ).…”

Section: Methodsmentioning

confidence: 99%

The inflammasome pathway in stable COPD and acute exacerbations

et al. 2016

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Chronic obstructive pulmonary disease (COPD) is characterised by pulmonary and systemic inflammation that bursts during exacerbations of the disease (ECOPD). The NLRP3 inflammasome is a key regulatory molecule of the inflammatory response. Its role in COPD is unclear.We investigated the NLRP3 inflammasome status in: 1) lung tissue samples from 38 patients with stable COPD, 15 smokers with normal spirometry and 14 never-smokers; and 2) sputum and plasma samples from 56 ECOPD patients, of whom 41 could be reassessed at clinical recovery.We observed that: 1) in lung tissue samples of stable COPD patients, NLRP3 and interleukin (IL)-1β mRNA were upregulated, but both caspase-1 and ASC were mostly in inactive form, and 2) during infectious ECOPD, caspase-1, oligomeric ASC and associated cytokines (IL-1β, IL-18) were significantly increased in sputum compared with clinical recovery.The NLRP3 inflammasome is primed, but not activated, in the lungs of clinically stable COPD patients. Inflammasome activation occurs during infectious ECOPD. The results of this study suggest that the inflammasome participates in the inflammatory burst of infectious ECOPD.

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Section: Methodsmentioning

confidence: 99%

The inflammasome pathway in stable COPD and acute exacerbations

et al. 2016

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“…Lung tissue samples were collected, processed and provided by the Lung Tissue Biobank of CIBERES ( http://www.ciberes.org), as described elsewhere [9]. They were obtained from volunteers that required lung resectional surgery because of clinical reasons, mostly lung cancer.…”

Section: Methodsmentioning

confidence: 99%

An investigation of the resolution of inflammation (catabasis) in COPD

et al. 2012

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BackgroundChronic Obstructive Pulmonary Disease (COPD) is characterized by an enhanced inflammatory response to smoking that persists despite quitting. The resolution of inflammation (catabasis) is a complex and highly regulated process where tissue resident macrophages play a key role since they phagocytose apoptotic cells (efferocytosis), preventing their secondary necrosis and the spill-over of their pro-inflammatory cytoplasmic content, and release pro-resolution and tissue repair molecules, such as TGFβ, VEGF and HGF. Because inflammation does not resolve in COPD, we hypothesized that catabasis may be abnormal in these patients.MethodsTo explore this hypothesis, we studied lung tissue samples obtained at surgery from 21 COPD patients, 22 smokers with normal spirometry and 13 non-smokers controls. In these samples we used: (1) immunohistochemistry to assess the expression of CD44, CD36, VEGF and TGFβ in lung macrophages; (2) real time PCR to determine HGF, PPARγ, TGFβ, VEGF and MMP-9 gene expression; and, (3) ELISA to quantify lipoxin A4, a lipid mediator of catabasis.ResultsWe found that current and former smokers with COPD showed: (1) more inflammation (higher MMP-9 expression); (2) reduced macrophage surface expression of CD44, a key efferocytosis receptor; and, (3) similar levels of TGFβ, VEGF, HGF, PPARγ, and lipoxin A4 than smokers with normal spirometry, despite the presence of inflammation and disease.ConclusionsThese results identify several potential abnormalities of catabasis in patients with COPD.

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“…However, it was also acknowledged that the design and statistical methods involved in a platform trial are complex, and that they would require appropriate knowledge and expertise. Finally, it was agreed that such a trial will create the opportunity to generate a multicentre biobank [78] to store biological samples for future studies.…”

Section: Trial Designmentioning

confidence: 99%

Precision medicine in airway diseases: moving to clinical practice

et al. 2017

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On February 21, 2017, a European Respiratory Society research seminar held in Barcelona discussed how to best apply precision medicine to chronic airway diseases such as asthma and chronic obstructive pulmonary disease. It is now clear that both are complex and heterogeneous diseases, that often overlap and that both require individualised assessment and treatment. This paper summarises the presentations and discussions that took place during the seminar. Specifically, we discussed the need for a new taxonomy of human diseases, the role of different players in this scenario (exposome, genes, endotypes, phenotypes, biomarkers and treatable traits) and a number of unanswered key questions in the field. We also addressed how to deploy airway precision medicine in clinical practice today, both in primary and specialised care. Finally, we debated the type of research needed to move the field forward.

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The CIBERES Pulmonary Biobank Consortium: an opportunity for cooperative international respiratory research

Cited by 9 publications

References 5 publications

The inflammasome pathway in stable COPD and acute exacerbations

The inflammasome pathway in stable COPD and acute exacerbations

An investigation of the resolution of inflammation (catabasis) in COPD

Precision medicine in airway diseases: moving to clinical practice

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