Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease

Abstract

Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD) [1][2][3]. The pathogenesis of smoke-induced COPD has been evaluated in a number of studies showing the accumulation of inflammatory cells in patients' airways: predominantly polymorphonuclear leukocytes in samples representative of intraluminal infla-mmation (sputum, bronchial and bronchoalveolar lavage) and mainly mononuclear cells, lymphocytes and macrophages, in tissue specimens [4][5][6][7][8][9][10][11][12][13].While the reason (or reasons) for this discrepancy is still not completely clear, these studies have opened the field to new questions. Since the relevance of airway inflammation in COPD has been demonstrated, the next step is the characterization of the different features of airway inflammation, such as the nature of chemotactic signal(s) and the contribution of the various cell types to airway inflammation through the release of inflammatory mediators.In this regard, this study was targeted on a COPD patient population of nonatopic current smokers with airway obstruction, with the aim of investigating the characteristics of intraluminal airway inflammation in these patients. Therefore, this study evaluated the presence in bronchial lavage (BL) of: interleukin (IL)-8, a chemotactic factor for polymorphonuclear cells into the airways; myeloperoxidase (MPO), eosinophil cationic protein (ECP) and tryptase, mediators of tissue damage from polymorphonuclear cells and mast cells; and the correlations between cellular and noncellular data obtained from BL. Materials and methods Study subjectsTwelve patients with COPD entered this study. They all had chronic productive cough for >3 months for 2 consecutive yrs, in the absence of other known disorders, such as bronchiectasis, tuberculosis or lung cancer [14,15]. The patients met the following inclusion criteria: 1) history of cigarette smoking, with a minimum of 15 pack-yrs, in patients who all were current smokers at time of evaluation; 2) no occupational or other exposure to other substances known to cause lung disorders; 3) absence of atopy, i.e. with negative skin tests for common allergen These data suggest that cigarette smoke is associated with increased amounts of airway interleukin-8, a chemotactic factor for neutrophils and eosinophils. Recruited neutrophils and eosinophils are activated and they release increased amounts of inflammatory mediators capable of damaging the bronchial tissue. Eur Respir J 1998; 12: 380-386

Imbalanced secretion of IL‐1β and IL‐1RA inChlamydia pneumoniae-infected mononuclear cells from COPD patients

“…Significantly enhanced IL-8 levels were found in C. pneumoniaeinfected and unstimulated AMs from COPD patients in the present study. Increased sputum levels of IL-8 associated with enhanced neutrophil activation have been previously reported during acute exacerbation in COPD patients [27,28]. The precise role of exacerbations in patients suffering from chronic obstructive lung disease in tissue destruction and FEV1 decline is still the subject of controversy.…”

Eosinophilic biomarkers for detection of acute exacerbation of chronic obstructive pulmonary disease with or without pulmonary embolism

“…Clinical investigations have reported that eosinophils are increased in the sputum and bronchial biopsies of patients with AECOPD (31,32). Increased levels of ECP in serum (24,33), bronchoalveolar lavage fluid (34) and induced sputum (35) have been observed in patients with AECOPD. Hospers et al (20) proposed that peripheral blood eosinophilia may also lead to a higher mortality rate for patients with AECOPD.…”

Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

“…For example, higher numbers of neutrophils, macrophages and CD8 positive T-cells in the peripheral airways of COPD patients were found as compared to smokers [10,[17][18][19], whereas others did not [10,19,20]. Two studies showed a higher percentage of neutrophils and higher IL-8 levels in broncho-alveolar lavage of COPD patients [13,21], whereas Linden et al found no differences [7]. A few studies showed higher numbers of neutrophils [22], CD3, CD4 [23] CD8 positive T-cells [23,24] in bronchial biopsies, whereas other studies found no differences in neutrophils [24], CD3, CD4 [22,24] and CD8 positive T-cels [22], macrophages, eosinophils and mast cells [22,24].…”