Extract
Elastin degradation in the lung, leading to emphysema, and elastin degradation in blood vessels, leading to atherosclerosis, are key mechanisms in the development and progression of chronic obstructive pulmonary disease (COPD) [1]. Elastin degradation can be measured in blood through quantification of desmosine and its isomer iso-demosine, which are released specifically through cleavage of mature elastin [2]. Severe COPD is frequently associated with chronic neutrophil-mediated inflammation and airway microbial dysbiosis [3]. Neutrophils release harmful proteases through the processes of degranulation and neutrophil extracellular trap formation that degrade extracellular matrix, including elastin, leading to disease progression [3, 4].
Abstract
Circulating desmosine is not reduced by treatment with azithromycin in COPD but elevated desmosine may identify a patient group with a greater treatment response http://ow.ly/vN6N30mhBA1
Footnotes
Author contributions: Conception and design: J.D. Chalmers, M. Schouten, H.R. Keir, J.T-J. Huang and M. van der Eerden. All authors participated in data analysis and interpretation of the data. All authors were involved in writing and revising the article prior to submission.
Conflict of interest: J.D. Chalmers reports grants and personal fees from GlaxoSmithKline (research grants for COPD), grants and personal fees from Boehringer Ingelheim (research grants for COPD studies), grants from AstraZeneca (research grants for COPD), grants and personal fees from Pfizer (research grants for COPD), grants and personal fees from Bayer Healthcare, and personal fees from Grifols and Napp, all outside the submitted work.
Conflict of interest: R.S. Djamin has nothing to disclose.
Conflict of interest: M. Schouten has nothing to disclose.
Conflict of interest: H.R. Keir has nothing to disclose.
Conflict of interest: B. Tan has nothing to disclose.
Conflict of interest: J.G.J.V. Aerts has nothing to disclose.
Conflict of interest: J.T-J. Huang has nothing to disclose.
Conflict of interest: M. van der Eerden has nothing to disclose.
Support statement: J.D. Chalmers is supported by the GlaxoSmithKline/British Lung Foundation Chair of Respiratory Research. The original COLUMBUS study was funded by the SoLong Trust. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received August 12, 2018.
- Accepted October 11, 2018.
- Copyright ©ERS 2018
This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.