Chest
Volume 123, Issue 4, April 2003, Pages 1054-1059
Journal home page for Chest

Clinical Investigations
COPD
The Cellular Composition and Macrophage Phenotype in Induced Sputum in Smokers and Ex-Smokers With COPD

https://doi.org/10.1378/chest.123.4.1054Get rights and content

Study objectives:

The relationship between smoking and COPD has been well-documented. We investigated the impact of cigarette smoking on airway inflammation in COPD patients.

Design:

Changes in cell profiles in induced sputum (IS) samples from smokers with COPD and patients who ceased smoking were compared.

Setting:

Department of pneumonology in a university hospital.

Patients:

IS samples were collected from 17 smokers and 17 ex-smokers with COPD.

Interventions:

We examined IS samples for differential cell counts and macrophage phenotypes determined by immunocytochemistry with monoclonal antibodies anti-CD11b, anti-CD14, anti-CD54, and anti-CD71.

Measurements and results:

The median IS volume was greater and the total cell count was higher in smokers than in ex-smokers. The difference, however, was not significant. We did not find any significant differences in the proportions of cells and in the phenotypes of macrophages between the two groups, with the proportion of eosinophils being slightly higher in the group of smokers. We found, however, a significant positive correlation between the decrease in pulmonary function parameters and the number of pack-years smoked, an inverse correlation of pulmonary function test results with the number of lymphocytes in IS, and a correlation between some changes in the expression of macrophage surface markers and smoking history. There was no correlation between the time from smoking cessation and any cellular component found in IS samples.

Conclusions:

The analysis of IS samples in patients with COPD revealed no significant differences in cell count and macrophage phenotypes between active smokers and ex-smokers.

Section snippets

Subjects

In this prospective study, 38 patients with COPD were included. The diagnosis of COPD was established according to the standards of the Global Initiative for Chronic Obstructive Lung Disease.1 We managed to obtain IS samples from 34 patients. The clinical characteristics of the population under study are presented in Table 1. Patients who had ceased smoking at least 1 year prior to entering the study were included in the group of ex-smokers. None of the subjects showed signs of infection during

Results

There were no significant differences in the severity of COPD, the median FEV1, median FVC, and median arterial blood gas levels in the two investigated groups (Table 2). In both groups, the pulmonary function parameters (ie, FEV1, FVC, and maximal expiratory flow at 50% of vital capacity), expressed as percent predicted values, correlated adversely with cigarette consumption, expressed as the number of pack-years. There was also a positive correlation between cigarette consumption and arterial

Discussion

This study showed that there are no significant differences in the cellular profile of IS samples between patients with COPD who are active smokers and those who have ceased smoking. To the best of our knowledge, ours is the first comparison between these groups of patients. In the majority of studies on IS samples from patients with COPD, what was compared was the sputum samples received from healthy subjects or a group of smokers with those from nonsmokers. There have been few studies of the

References (28)

  • M Saetta et al.

    Cellular and structural bases of chronic obstructive pulmonary disease

    Am J Respir Crit Care Med

    (2001)
  • D Stanescu et al.

    Airways obstruction, chronic expectoration, and rapid decline of FEV1 in smokers are associated with increased levels of sputum neutrophils

    Thorax

    (1996)
  • L Jayaram et al.

    Induced sputum cell counts: their usefulness in clinical practice

    Eur Respir J

    (2000)
  • C Lensmar et al.

    Leukocyte counts and macrophage phenotypes in induced sputum and bronchoalveolar lavage fluid from normal subjects

    Eur Respir J

    (1998)
  • Cited by (0)

    View full text