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Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD

BACKGROUND: Smoking activates and recruits inflammatory cells and proteases to the airways. Matrix metalloproteinase (MMP)-12 may be a key mediator in smoke induced emphysema. However, the influence of smoking and its cessation on airway inflammation and MMP-12 expression during COPD is still unknow...

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Autores principales: Babusyte, Agne, Stravinskaite, Kristina, Jeroch, Jolanta, Lötvall, Jan, Sakalauskas, Raimundas, Sitkauskiene, Brigita
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2200652/
https://www.ncbi.nlm.nih.gov/pubmed/18001475
http://dx.doi.org/10.1186/1465-9921-8-81
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author Babusyte, Agne
Stravinskaite, Kristina
Jeroch, Jolanta
Lötvall, Jan
Sakalauskas, Raimundas
Sitkauskiene, Brigita
author_facet Babusyte, Agne
Stravinskaite, Kristina
Jeroch, Jolanta
Lötvall, Jan
Sakalauskas, Raimundas
Sitkauskiene, Brigita
author_sort Babusyte, Agne
collection PubMed
description BACKGROUND: Smoking activates and recruits inflammatory cells and proteases to the airways. Matrix metalloproteinase (MMP)-12 may be a key mediator in smoke induced emphysema. However, the influence of smoking and its cessation on airway inflammation and MMP-12 expression during COPD is still unknown. We aimed to analyse airway inflammatory cell patterns in induced sputum (IS) and bronchoalveolar lavage (BAL) from COPD patients who are active smokers and who have ceased smoking >2 years ago. METHODS: 39 COPD outpatients – smokers (n = 22) and ex-smokers (n = 17) were studied. 8 'healthy' smokers and 11 healthy never-smokers were tested as the control groups. IS and BAL samples were obtained for differential and MMP-12(+)-macrophages count analysis. RESULTS: The number of IS neutrophils was higher in both COPD groups compared to both controls. The amount of BAL neutrophils was higher in COPD smokers compared to healthy never-smokers. The number of BAL MMP-12(+)-macrophages was higher in COPD smokers (1.6 ± 0.3 × 10(6)/ml) compared to COPD ex-smokers, 'healthy' smokers and healthy never-smokers (0.9 ± 0.4, 0.4 ± 0.2, 0.2 ± 0.1 × 10(6)/ml respectively, p < 0.05). CONCLUSION: The lower amount of BAL neutrophils in COPD ex-smokers, compared to COPD smokers, suggests positive alterations in alveolar compartment after smoking cessation. Smoking and disease itself may stimulate MMP-12 expression in airway compartments (IS and BAL) from COPD patients.
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spelling pubmed-22006522008-01-16 Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD Babusyte, Agne Stravinskaite, Kristina Jeroch, Jolanta Lötvall, Jan Sakalauskas, Raimundas Sitkauskiene, Brigita Respir Res Research BACKGROUND: Smoking activates and recruits inflammatory cells and proteases to the airways. Matrix metalloproteinase (MMP)-12 may be a key mediator in smoke induced emphysema. However, the influence of smoking and its cessation on airway inflammation and MMP-12 expression during COPD is still unknown. We aimed to analyse airway inflammatory cell patterns in induced sputum (IS) and bronchoalveolar lavage (BAL) from COPD patients who are active smokers and who have ceased smoking >2 years ago. METHODS: 39 COPD outpatients – smokers (n = 22) and ex-smokers (n = 17) were studied. 8 'healthy' smokers and 11 healthy never-smokers were tested as the control groups. IS and BAL samples were obtained for differential and MMP-12(+)-macrophages count analysis. RESULTS: The number of IS neutrophils was higher in both COPD groups compared to both controls. The amount of BAL neutrophils was higher in COPD smokers compared to healthy never-smokers. The number of BAL MMP-12(+)-macrophages was higher in COPD smokers (1.6 ± 0.3 × 10(6)/ml) compared to COPD ex-smokers, 'healthy' smokers and healthy never-smokers (0.9 ± 0.4, 0.4 ± 0.2, 0.2 ± 0.1 × 10(6)/ml respectively, p < 0.05). CONCLUSION: The lower amount of BAL neutrophils in COPD ex-smokers, compared to COPD smokers, suggests positive alterations in alveolar compartment after smoking cessation. Smoking and disease itself may stimulate MMP-12 expression in airway compartments (IS and BAL) from COPD patients. BioMed Central 2007 2007-11-14 /pmc/articles/PMC2200652/ /pubmed/18001475 http://dx.doi.org/10.1186/1465-9921-8-81 Text en Copyright © 2007 Babusyte et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Babusyte, Agne
Stravinskaite, Kristina
Jeroch, Jolanta
Lötvall, Jan
Sakalauskas, Raimundas
Sitkauskiene, Brigita
Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title_full Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title_fullStr Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title_full_unstemmed Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title_short Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
title_sort patterns of airway inflammation and mmp-12 expression in smokers and ex-smokers with copd
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2200652/
https://www.ncbi.nlm.nih.gov/pubmed/18001475
http://dx.doi.org/10.1186/1465-9921-8-81
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