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ERJ Open Res. 2016 Jul 11;2(3). pii: 00002-2016. eCollection 2016 Jul.

The inflammasome pathway in stable COPD and acute exacerbations.

Author information

1
Fundació Clinic per a la Recerca Biomèdica, Barcelona, Spain; CIBER Respiratory Diseases (CIBERES), Barcelona, Spain; These authors contributed equally to this work.
2
CIBER Respiratory Diseases (CIBERES), Barcelona, Spain; Pulmonary Service, Hospital Txagorritxu, Vitoria, Spain; These authors contributed equally to this work.
3
CIBER Respiratory Diseases (CIBERES), Barcelona, Spain; University Hospital Son Espases-IdISPa, Palma de Mallorca, Spain.
4
University Hospital Son Espases-IdISPa, Palma de Mallorca, Spain.
5
Fundació Clinic per a la Recerca Biomèdica, Barcelona, Spain; CIBER Respiratory Diseases (CIBERES), Barcelona, Spain.
6
Institut Respiratori, Hospital Clinic, Barcelona, Spain; Biomedic Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
7
Biomedic Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Immunology Dept, Hospital Clinic, Barcelona, Spain.
8
Inflammation and Experimental Surgery Unit, CIBERHED, Murcia's BioHealth, Research Institute IMIB-Arrixaca, University Hospital Virgen de la Arrixaca, Murcia, Spain.
9
CIBER Respiratory Diseases (CIBERES), Barcelona, Spain; Institut Respiratori, Hospital Clinic, Barcelona, Spain; Biomedic Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
10
Fundació Clinic per a la Recerca Biomèdica, Barcelona, Spain; CIBER Respiratory Diseases (CIBERES), Barcelona, Spain; Institut Respiratori, Hospital Clinic, Barcelona, Spain; Biomedic Research Institute August Pi i Sunyer (IDIBAPS), Barcelona, Spain.

Abstract

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.

Conflict of interest statement

can be found alongside this article at openres.ersjournals.com

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