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

Myeloperoxidase as a marker of increasing systemic inflammation in smokers without severe airway symptoms
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DOI:
10.1016/j.rmed.2006.09.023
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发表时间:
2007-05-01
影响因子:
4.3
通讯作者:
Ekberg-Jansson, Ann
Ekberg-Jansson, Ann
中科院分区:
医学3区
文献类型:
--
作者:
Andelid, Kristina;Bake, Bjorn;Ekberg-Jansson, Ann

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背景:有越来越多的证据表明慢性阻塞性肺疾病(COPD)患者存在全身炎症,但关于无严重呼吸道症状的吸烟者全身炎症发展的信息很少。在这项纵向研究中,我们通过对吸烟者血液中炎症标志物的检测,检查了有轻度或无呼吸道症状的吸烟者在6年内是否出现了全身炎症的迹象。方法:在1995年(0年)和6年后(6年)对40名吸烟者和28名从不吸烟的配偶进行了调查。在第6年,有11名吸烟者(戒烟者)戒烟;这些受试者被作为一个单独的组进行分析。在第0和第6年,我们检测了血清髓过氧化物酶(MPO)、溶菌酶和人中性粒细胞Lipocalin(HNL)的水平,作为中性粒细胞和单核细胞系细胞、单核细胞系细胞和仅中性粒细胞的活性标志。结果:在第6年吸烟者的所有系统炎症标志物(MPO、HNL和溶菌酶)都显著高于不吸烟者。尽管戒烟者的MPO没有表现出任何明显的变化,但我们观察到在这一组中,血液MPO的变化与戒烟持续时间之间存在显著的负相关。对于HNL和溶菌酶,吸烟者和从不吸烟者随时间的变化相似,与戒烟者相比没有统计学意义。结论:本研究提供了证据,表明没有严重呼吸道症状的男性吸烟者在6年内发生了日益严重的全身炎症。这项研究提供了直接和间接的证据,表明MPO可能是这种全身炎症的早期标志。然而,我们的研究也提供了间接证据,表明持续吸烟可能会“推动”全身HNL和溶菌酶的水平。MPO升高的来源及其作为预测未来COPD的一个容易测量的指标的价值值得进一步评估。(C)2006爱思唯尔有限公司。保留所有权利。
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 mate 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-tineage 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 atone, 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. (C) 2006 Elsevier Ltd. All rights reserved.