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Introduction <p>Cigarette smoking is a major driver of airway and systemic inflammation and contributes to the development and progression of chronic obstructive pulmonary disease (COPD). This study compared peripheral blood inflammatory markers and immune cell profiles in smokers with and without COPD and in non-smoking controls.</p> Methods <p>In this cross-sectional study, blood samples were collected from 80 participants (<i>n</i> = 20/group): non-smoker controls (NS), smokers with normal lung function (NLFS), current smokers with COPD (COPD-CS), and ex-smokers with COPD (COPD-ES). Total white cell count (WCC) and leukocyte differentials (neutrophils, lymphocytes, monocytes, eosinophils) were measured using an automated haematology analyser (Sysmex XN2000). Systemic inflammatory markers were measured using&#xa0;C-reactive protein (CRP, Roche Cobas Pro) and erythrocyte sedimentation rate (ESR, Diesse VES-MATIC Easy). Lung function parameters (including FEV1, FVC, DLco, FEF25–75%, and SpO2) were assessed and correlated with blood markers.</p> Results <p>Compared with NS, WCC, neutrophils, and monocytes were higher in both COPD groups and in NLFS (all <i>p</i> &lt; 0.05). Lymphocytes were higher in NLFS and COPD-CS (<i>p</i> &lt; 0.05). Eosinophils were higher in COPD-ES and NLFS relative to NS (<i>p </i>&lt; 0.05). ESR and CRP were elevated in NLFS and both COPD groups compared with NS (<i>p</i> &lt; 0.05). In COPD, higher blood inflammatory cell counts were associated with poorer lung function (negative correlations; <i>p</i> &lt; 0.05).</p> Conclusion <p>Peripheral blood inflammatory markers are increased in smokers, including those with preserved lung function, and in COPD. Differences in eosinophil patterns between COPD current smokers and ex-smokers suggest inflammatory heterogeneity and should be confirmed in larger, well-characterized cohorts. These findings support the move towards careful personalized medicine interventions, based on individual inflammatory profiles.</p>

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Peripheral Blood Inflammatory Markers and Immune Cell Profiles in Smokers With and Without COPD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月20日

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  • Wenying Lu,
  • Maddison Waters,
  • Josie Larby,
  • Sapha Shibeeb,
  • Steven Bozinovski,
  • Stavros Selemidis,
  • Jonathan McQualter,
  • Ross Vlahos,
  • Md Imtaiyaz Hassan,
  • Heinrich Weber,
  • Sukhwinder Singh Sohal

摘要

Introduction

Cigarette smoking is a major driver of airway and systemic inflammation and contributes to the development and progression of chronic obstructive pulmonary disease (COPD). This study compared peripheral blood inflammatory markers and immune cell profiles in smokers with and without COPD and in non-smoking controls.

Methods

In this cross-sectional study, blood samples were collected from 80 participants (n = 20/group): non-smoker controls (NS), smokers with normal lung function (NLFS), current smokers with COPD (COPD-CS), and ex-smokers with COPD (COPD-ES). Total white cell count (WCC) and leukocyte differentials (neutrophils, lymphocytes, monocytes, eosinophils) were measured using an automated haematology analyser (Sysmex XN2000). Systemic inflammatory markers were measured using C-reactive protein (CRP, Roche Cobas Pro) and erythrocyte sedimentation rate (ESR, Diesse VES-MATIC Easy). Lung function parameters (including FEV1, FVC, DLco, FEF25–75%, and SpO2) were assessed and correlated with blood markers.

Results

Compared with NS, WCC, neutrophils, and monocytes were higher in both COPD groups and in NLFS (all p < 0.05). Lymphocytes were higher in NLFS and COPD-CS (p < 0.05). Eosinophils were higher in COPD-ES and NLFS relative to NS (p < 0.05). ESR and CRP were elevated in NLFS and both COPD groups compared with NS (p < 0.05). In COPD, higher blood inflammatory cell counts were associated with poorer lung function (negative correlations; p < 0.05).

Conclusion

Peripheral blood inflammatory markers are increased in smokers, including those with preserved lung function, and in COPD. Differences in eosinophil patterns between COPD current smokers and ex-smokers suggest inflammatory heterogeneity and should be confirmed in larger, well-characterized cohorts. These findings support the move towards careful personalized medicine interventions, based on individual inflammatory profiles.