Granulocyte activation markers in induced sputum: comparison between chronic obstructive pulmonary disease, asthma, and normal subjects.

Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 11.99). 03/1997; 155(2):449-53. DOI: 10.1164/ajrccm.155.2.9032177
Source: PubMed

ABSTRACT Airway inflammation is present in asthma and is thought to play a significant part in the development of airflow obstruction. In chronic obstructive pulmonary disease (COPD), neutrophilic inflammation is present in the airway lumen, whereas the submucosa displays a lymphocytic infiltrate. Less is known about the nature and mechanisms of inflammation in COPD than in asthma. Induced sputum allows noninvasive sampling of respiratory tract secretions from patients and control subjects, allowing characterization of cells and measurement of soluble markers. We exploited this technique in order to compare the presence and quantify specific markers of eosinophil and neutrophil activation in subjects with asthma or COPD, and control subjects. Differential cell counts showed significantly higher neutrophil percentages in the patients with COPD compared with other groups, while patients with asthma had higher numbers of eosinophils. The neutrophil markers myeloperoxidase (MPO), from primary granules in neutrophils, and human neutrophil lipocalin (HNL), released from secondary granules, were elevated in patients with asthma and COPD compared with control subjects but markedly more so in COPD. The difference between COPD and asthma was more marked for HNL than for MPO suggesting that HNL may be a better marker for discriminating between these conditions. Concentrations of the eosinophil granule protein, eosinophil cationic protein (ECP), and the eosinophil granule-derived enzyme, eosinophil peroxidase (EPO) were raised in the patients with asthma and those with COPD.

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    ABSTRACT: Aim of the work This study aimed to analyze induced sputum in asthmatic patients under different forms of treatment and study factors that may affect sputum cellularity in asthmatic patients. Patients and methods Eighty asthmatic patients were included. Patients with contra-indication for sputum induction were excluded. Spirometer, sputum induction, sputum processing, sputum total cell count, viability, centrifugation, staining and count were done. Results Eighty patients were included in the study to investigate induced sputum in asthmatic patients under different forms of treatment. Patient’s sex 43 (53.8%) male and 37 (46.2%) female patients were included. Their mean age ± SD was 32.05 ± 10.87 years. Sputum cell indices of asthmatic patients were 35.22% neutrophilic inflammation, 17.81% eosinophilic inflammation and the lymphocytic inflammation was 26.48%. Conclusion Study concluded that the use of sputum induction as noninvasive measurements of airway inflammation in the diagnosis and management of asthma is very important for every patient diagnosed with bronchial asthma before starting asthma management and for asthmatic patients who were not controlled by full asthma management to understand the type of airway inflammation.
    01/2013; 63(1). DOI:10.1016/j.ejcdt.2013.11.008
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) currently ranks as the fourth cause of death in the United States and it is an increasingly important health problem for the rest of the world [1-3]. Its prevalence has increased as overall mortality from myocardial infarction and cerebro-vascular accident, the two organ system affected by the same risk factor (namely cigarette smoking), have decreased. Although preventable and treatable, once diagnosed and sympto-matic COPD is progressive and in some patients leads to disability usually due to dyspnea, at a relatively early age (6 th or 7 th decade) [4,5]. Limitation to airflow occurs as a consequence of destruction of lung parenchyma or to alterations in the airway itself. One of the most important consequences is the development of static and dynamic hyperinflation with im-portant clinical consequences such as dyspnea with exercise and decreased survival. This chapter integrates the pathologic changes of COPD with the known adaptive and maladaptive consequences of those changes. These factors should help us understand the rationale behind the therapeutic strategies aimed at decreasing lung volume and addressing the complica-tions of patients with COPD. DEFINITION COPD is a preventable and treatable disease state charac-terized by the presence of airflow obstruction due to emphy-sema or intrinsic airway disease. The airflow limitation is associated with an abnormal inflammatory response to in-haled particles or noxious gases (mainly cigarette smoking). COPD may be associated with important systemic conse-quences [4, 5]. The obstruction to airflow is generally pro-gressive, may be accompanied by airway hyperactivity and may be partially reversible. In this chapter we will only ad-dress the pulmonary expression of COPD and not touch on the systemic manifestations of the disease. Emphysema is defined pathologically as an abnormal permanent enlargement of the air spaces distal to the termi-nal bronchioles, accompanied by destruction of their walls, without prominent fibrosis. Airways disease is though to be-gin primarily in the small airways (measuring around 2 mm) but also affect the gland containing airways leading to chronic bronchitis with the frequent increase in mucous pro-duction and the development of cough. In most patients with COPD involvement of the airways and parenchymal destruc-tion coexist simultaneously [4,5]. The disease does not affect all portions of the lung to the same degree. This uneven dis-tribution influences the physiologic behavior of different parts of the lung and its structures, leading to uneven ventila-tion perfusion and gas exchange as we shall discuss below.
    Current Respiratory Medicine Reviews 11/2008; 4(4). DOI:10.2174/157339808786263734
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    ABSTRACT: The pathogenesis of asthma and chronic obstructive pulmonary disease (COPD) has been claimed to be attributable to increased systemic and local oxidative stress. Detection of the oxidant burden and evaluation of their progression and phenotypes by oxidant biomarkers have proved challenging and difficult. A large number of asthmatics are cigarette smokers and smoke itself contains oxidants complicating further the use of oxidant biomarkers. One of the most widely used oxidant markers in asthma is exhaled nitric oxide (NO), which plays an important role in the pathogenesis of asthma and disease monitoring. Another oxidant marker that has been widely investigated in COPD is 8-isoprostane, but it is probably not capable of differentiating asthma from COPD, or even sensitive in the early assessment of these diseases. None of the current biomarkers have been shown to be better than exhaled NO in asthma. There is a need to identify new biomarkers for obstructive airway diseases, especially their differential diagnosis. A comprehensive evaluation of oxidant markers and their combinations will be presented in this review. In brief, it seems that additional analyses utilizing powerful tools such as genomics, metabolomics, lipidomics, and proteomics will be required to improve the specificity and sensitivity of the next generation of biomarkers.
    International Journal of COPD 02/2008; 3(4):585-603. · 2.73 Impact Factor