Persistence of circulating endothelial microparticles in COPD despite smoking cessation

Yael Strulovici-Barel, Michelle R. Staudt, Anja Krause, Cynthia Gordon, Ann E. Tilley, Ben Gary Harvey, Robert J. Kaner, Charleen Hollmann, Jason G. Mezey, Hans Bitter, Sreekumar G. Pillai, Holly Hilton, Gerhard Wolff, Christopher S. Stevenson, Sudha Visvanathan, Jay S. Fine, Ronald Crystal

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Introduction Increasing evidence links COPD pathogenesis with pulmonary capillary apoptosis. We previously demonstrated that plasma levels of circulating microparticles released from endothelial cells (EMPs) due to apoptosis are elevated in smokers with normal spirometry but low diffusion capacity, that is, with early evidence of lung destruction. We hypothesised that pulmonary capillary apoptosis persists with the development of COPD and assessed its reversibility in healthy smokers and COPD smokers following smoking cessation. Methods Pulmonary function and high-resolution CT (HRCT) were assessed in 28 non-smokers, 61 healthy smokers and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers quit smoking for 12 months following the baseline visit. Total EMP (CD42b-CD31+), pulmonary capillary EMP (CD42b-CD31+ACE+) and apoptotic EMP (CD42b-CD62E+/CD42b-CD31+) levels were quantified by flow cytometry. Results Compared with non-smokers, healthy smokers and COPD smokers had elevated levels of circulating EMPs due to active pulmonary capillary endothelial apoptosis. Levels remained elevated over 12 months in healthy smokers and COPD smokers who continued smoking, but returned to non-smoker levels in healthy smokers who quit. In contrast, levels remained significantly abnormal in COPD smokers who quit. Conclusions Pulmonary capillary apoptosis is reversible in healthy smokers who quit, but continues to play a role in COPD pathogenesis in smokers who progressed to airflow obstruction despite smoking cessation.

Original languageEnglish
Pages (from-to)1137-1144
Number of pages8
JournalThorax
Volume71
Issue number12
DOIs
Publication statusPublished - 1 Dec 2016
Externally publishedYes

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Smoking Cessation
Chronic Obstructive Pulmonary Disease
Lung
Apoptosis
Smoking
Spirometry
Flow Cytometry
Endothelial Cells

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Strulovici-Barel, Y., Staudt, M. R., Krause, A., Gordon, C., Tilley, A. E., Harvey, B. G., ... Crystal, R. (2016). Persistence of circulating endothelial microparticles in COPD despite smoking cessation. Thorax, 71(12), 1137-1144. https://doi.org/10.1136/thoraxjnl-2015-208274

Persistence of circulating endothelial microparticles in COPD despite smoking cessation. / Strulovici-Barel, Yael; Staudt, Michelle R.; Krause, Anja; Gordon, Cynthia; Tilley, Ann E.; Harvey, Ben Gary; Kaner, Robert J.; Hollmann, Charleen; Mezey, Jason G.; Bitter, Hans; Pillai, Sreekumar G.; Hilton, Holly; Wolff, Gerhard; Stevenson, Christopher S.; Visvanathan, Sudha; Fine, Jay S.; Crystal, Ronald.

In: Thorax, Vol. 71, No. 12, 01.12.2016, p. 1137-1144.

Research output: Contribution to journalArticle

Strulovici-Barel, Y, Staudt, MR, Krause, A, Gordon, C, Tilley, AE, Harvey, BG, Kaner, RJ, Hollmann, C, Mezey, JG, Bitter, H, Pillai, SG, Hilton, H, Wolff, G, Stevenson, CS, Visvanathan, S, Fine, JS & Crystal, R 2016, 'Persistence of circulating endothelial microparticles in COPD despite smoking cessation', Thorax, vol. 71, no. 12, pp. 1137-1144. https://doi.org/10.1136/thoraxjnl-2015-208274
Strulovici-Barel Y, Staudt MR, Krause A, Gordon C, Tilley AE, Harvey BG et al. Persistence of circulating endothelial microparticles in COPD despite smoking cessation. Thorax. 2016 Dec 1;71(12):1137-1144. https://doi.org/10.1136/thoraxjnl-2015-208274
Strulovici-Barel, Yael ; Staudt, Michelle R. ; Krause, Anja ; Gordon, Cynthia ; Tilley, Ann E. ; Harvey, Ben Gary ; Kaner, Robert J. ; Hollmann, Charleen ; Mezey, Jason G. ; Bitter, Hans ; Pillai, Sreekumar G. ; Hilton, Holly ; Wolff, Gerhard ; Stevenson, Christopher S. ; Visvanathan, Sudha ; Fine, Jay S. ; Crystal, Ronald. / Persistence of circulating endothelial microparticles in COPD despite smoking cessation. In: Thorax. 2016 ; Vol. 71, No. 12. pp. 1137-1144.
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abstract = "Introduction Increasing evidence links COPD pathogenesis with pulmonary capillary apoptosis. We previously demonstrated that plasma levels of circulating microparticles released from endothelial cells (EMPs) due to apoptosis are elevated in smokers with normal spirometry but low diffusion capacity, that is, with early evidence of lung destruction. We hypothesised that pulmonary capillary apoptosis persists with the development of COPD and assessed its reversibility in healthy smokers and COPD smokers following smoking cessation. Methods Pulmonary function and high-resolution CT (HRCT) were assessed in 28 non-smokers, 61 healthy smokers and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers quit smoking for 12 months following the baseline visit. Total EMP (CD42b-CD31+), pulmonary capillary EMP (CD42b-CD31+ACE+) and apoptotic EMP (CD42b-CD62E+/CD42b-CD31+) levels were quantified by flow cytometry. Results Compared with non-smokers, healthy smokers and COPD smokers had elevated levels of circulating EMPs due to active pulmonary capillary endothelial apoptosis. Levels remained elevated over 12 months in healthy smokers and COPD smokers who continued smoking, but returned to non-smoker levels in healthy smokers who quit. In contrast, levels remained significantly abnormal in COPD smokers who quit. Conclusions Pulmonary capillary apoptosis is reversible in healthy smokers who quit, but continues to play a role in COPD pathogenesis in smokers who progressed to airflow obstruction despite smoking cessation.",
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AU - Staudt, Michelle R.

AU - Krause, Anja

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AU - Tilley, Ann E.

AU - Harvey, Ben Gary

AU - Kaner, Robert J.

AU - Hollmann, Charleen

AU - Mezey, Jason G.

AU - Bitter, Hans

AU - Pillai, Sreekumar G.

AU - Hilton, Holly

AU - Wolff, Gerhard

AU - Stevenson, Christopher S.

AU - Visvanathan, Sudha

AU - Fine, Jay S.

AU - Crystal, Ronald

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N2 - Introduction Increasing evidence links COPD pathogenesis with pulmonary capillary apoptosis. We previously demonstrated that plasma levels of circulating microparticles released from endothelial cells (EMPs) due to apoptosis are elevated in smokers with normal spirometry but low diffusion capacity, that is, with early evidence of lung destruction. We hypothesised that pulmonary capillary apoptosis persists with the development of COPD and assessed its reversibility in healthy smokers and COPD smokers following smoking cessation. Methods Pulmonary function and high-resolution CT (HRCT) were assessed in 28 non-smokers, 61 healthy smokers and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers quit smoking for 12 months following the baseline visit. Total EMP (CD42b-CD31+), pulmonary capillary EMP (CD42b-CD31+ACE+) and apoptotic EMP (CD42b-CD62E+/CD42b-CD31+) levels were quantified by flow cytometry. Results Compared with non-smokers, healthy smokers and COPD smokers had elevated levels of circulating EMPs due to active pulmonary capillary endothelial apoptosis. Levels remained elevated over 12 months in healthy smokers and COPD smokers who continued smoking, but returned to non-smoker levels in healthy smokers who quit. In contrast, levels remained significantly abnormal in COPD smokers who quit. Conclusions Pulmonary capillary apoptosis is reversible in healthy smokers who quit, but continues to play a role in COPD pathogenesis in smokers who progressed to airflow obstruction despite smoking cessation.

AB - Introduction Increasing evidence links COPD pathogenesis with pulmonary capillary apoptosis. We previously demonstrated that plasma levels of circulating microparticles released from endothelial cells (EMPs) due to apoptosis are elevated in smokers with normal spirometry but low diffusion capacity, that is, with early evidence of lung destruction. We hypothesised that pulmonary capillary apoptosis persists with the development of COPD and assessed its reversibility in healthy smokers and COPD smokers following smoking cessation. Methods Pulmonary function and high-resolution CT (HRCT) were assessed in 28 non-smokers, 61 healthy smokers and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers quit smoking for 12 months following the baseline visit. Total EMP (CD42b-CD31+), pulmonary capillary EMP (CD42b-CD31+ACE+) and apoptotic EMP (CD42b-CD62E+/CD42b-CD31+) levels were quantified by flow cytometry. Results Compared with non-smokers, healthy smokers and COPD smokers had elevated levels of circulating EMPs due to active pulmonary capillary endothelial apoptosis. Levels remained elevated over 12 months in healthy smokers and COPD smokers who continued smoking, but returned to non-smoker levels in healthy smokers who quit. In contrast, levels remained significantly abnormal in COPD smokers who quit. Conclusions Pulmonary capillary apoptosis is reversible in healthy smokers who quit, but continues to play a role in COPD pathogenesis in smokers who progressed to airflow obstruction despite smoking cessation.

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