Document Detail


Myeloperoxidase as a marker of increasing systemic inflammation in smokers without severe airway symptoms.
MedLine Citation:
PMID:  17098408     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: There is increasing evidence of systemic inflammation in patients with chronic obstructive pulmonary disease (COPD), but there is very little information on the development of systemic inflammation in smokers without severe airway symptoms. In this longitudinal study, we examined whether smokers with mild or no airway symptoms develop signs of systemic inflammation by assessing inflammatory markers in blood over a 6-year period. METHODS: Forty smokers and 28 male never-smokers were investigated in 1995 (year 0) and 6 years later (year 6). At year 6, 11 smokers had stopped smoking (quitters); these subjects were analysed as a separate group. At year 0 and 6, we measured serum levels of myeloperoxidase (MPO), lysozyme and human neutrophil lipocalin (HNL), regarded as markers of activity in neutrophils plus monocyte-lineage cells, monocyte-lineage cells only and neutrophils only. RESULTS: All systemic markers of inflammation (MPO, HNL and lysozyme) were significantly higher in smokers than in never smokers at year 6. For MPO alone, smokers only displayed a unique pattern compared with the other groups; the concentration of MPO in blood increased among smokers during the 6-year period, and this increase was statistically significant compared with that observed in never-smokers. Even though quitters did not display any clear change in MPO, we observed a statistically significant negative correlation between the change in blood MPO and the duration of smoking cessation in this group. For HNL and lysozyme, the changes over time were similar in smokers and never-smokers, with no statistically significant difference compared with quitters. CONCLUSION: This study provides evidence that male smokers without severe airway symptoms develop an increasing systemic inflammation during a 6-year period. The study forwards both direct and indirect evidence that MPO may be an early marker of this systemic inflammation. However, our study also forwards indirect evidence that ongoing tobacco smoking may "drive" the level of systemic HNL and lysozyme. The origin of the increased MPO and its value as an easily measured predictor for future COPD deserves to be further evaluated.
Authors:
Kristina Andelid; Björn Bake; Sabina Rak; Anders Lindén; Annika Rosengren; Ann Ekberg-Jansson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-13
Journal Detail:
Title:  Respiratory medicine     Volume:  101     ISSN:  0954-6111     ISO Abbreviation:  Respir Med     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-04-06     Completed Date:  2007-06-05     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8908438     Medline TA:  Respir Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  888-95     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine/Respiratory Medicine and Allergology, Sahlgrenska Academy at Göteborg University, Sweden. kristina.andelid@lungall.gu.se
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MeSH Terms
Descriptor/Qualifier:
Acute-Phase Proteins
Aged
Biological Markers / blood
Body Height
Body Mass Index
Follow-Up Studies
Forced Expiratory Volume
Humans
Inflammation / diagnosis,  enzymology,  etiology*,  physiopathology
Lipocalins
Male
Muramidase / blood
Peroxidase / blood*
Proto-Oncogene Proteins / blood
Pulmonary Diffusing Capacity
Respiratory Function Tests
Smoking / adverse effects*,  blood,  physiopathology
Smoking Cessation
Time Factors
Chemical
Reg. No./Substance:
0/Acute-Phase Proteins; 0/Biological Markers; 0/LCN2 protein, human; 0/Lipocalins; 0/Proto-Oncogene Proteins; EC 1.11.1.7/Peroxidase; EC 3.2.1.17/Muramidase

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