Myeloperoxidase as a marker of increasing systemic inflammation in smokers without severe airway symptoms.
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.


CONCLUSIONS
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.
Andelid
Kristina
K
Department of Internal Medicine/Respiratory Medicine and Allergology, Sahlgrenska Academy at Göteborg University, Sweden. kristina.andelid@lungall.gu.se
Bake
Björn
B
Rak
Sabina
S
Lindén
Anders
A
Rosengren
Annika
A
Ekberg-Jansson
Ann
A
D000209:Acute-Phase Proteins; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001827:Body Height; D015992:Body Mass Index; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000175:diagnosis / Q000201:enzymology / Q000209:etiology* / Q000503:physiopathology; D000071068:Lipocalin-2; D054834:Lipocalins; D008297:Male; D009113:Muramidase / Q000097:blood; D009195:Peroxidase / Q000097:blood*; D011518:Proto-Oncogene Proteins / Q000097:blood; D011653:Pulmonary Diffusing Capacity; D012129:Respiratory Function Tests; D012907:Smoking / Q000009:adverse effects* / Q000097:blood / Q000503:physiopathology; D016540:Smoking Cessation; D013997:Time Factors
D000209:Acute-Phase Proteins; D015415:Biomarkers; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D009195:Peroxidase; D009113:Muramidase