Abstract
In smoking COPD patients the bronchoalveolar lavage (BAL) fluid contains high numbers of inflammatory cells. These cells might produce arachidonic acid (AA) metabolites, which contribute to inflammation and an increased bronchomotor tone. To investigate levels of AA metabolites in BAL fluid, before and after inhaled glucocorticoid therapy: fluticasone propionate (FP) 1 mg per day, or placebo. A double-blind placebo controlled trial lasting six months. COPD patients were selected by clinical criteria and the presence of bronchial hyper-responsiveness (BHR). Lung function was recorded and in BAL fluid we counted cell numbers and measured LTB4, LTC4/D4/E4, PGE2, 6kPGF1alpha, PGF2alpha and TxB2. A control group consisted of asymptomatic smokers (n=6). Paired data were obtained from 9 FP treated and 11 placebo patients. BAL cells were almost exclusively alveolar macrophages. In patients and controls both cellularity and levels of AA metabolites were equal Cell numbers did not change after treatment. Statistically significant decreases after FP therapy were noticed for PGE2 (30%), 6kPGF1alpha (41%) and PGF2alpha (54%). In COPD, the capability of inflammatory cells to produce certain AA metabolites was decreased after inhaled FP treatment. This result is discussed in its relation to clinical effects, the influence of smoking, and the results of an earlier, similar study in asthma patients.
Highlights
Leukotrienes (LTs) and prostaglandins (PGs) are mediators of inflammation that have been investigated almost exclusively in asthma, but not in chronic obstructive pulmonary disease (COPD)
Leukotrienes (LTs) and prostaglandins (PGs) are mediators of inflammation that have been investigated almost exclusively in asthma, but not in COPD. These metabolites of arachidonic acid (AA) are products of several inflammatory cells and part of the mechanisms leading to bronchoconstriction and increased bronchomotor tone
In chronic obstructive pulmonary disease (COPD) airway narrowing is caused by several mechanisms, including mechanical factors, increased thickness of the walls of the conducting airways, increased bronchomotor tone and intraluminal secretions.[1,2]
Summary
Leukotrienes (LTs) and prostaglandins (PGs) are mediators of inflammation that have been investigated almost exclusively in asthma, but not in COPD. In chronic obstructive pulmonary disease (COPD) airway narrowing is caused by several mechanisms, including mechanical factors (loss of elasticity of the lung parenchyma), increased thickness of the walls of the conducting airways, increased bronchomotor tone and intraluminal secretions.[1,2] Increased numbers of alveolar macrophages, neutrophilic granulocytes and CD8 positive cells constitute the main burden of the cellular infiltrate in the airway walls and alveoli Their secretory products cause multiple effects, for instance cell influx and cell activation, and an increase of the contractile status of the smooth muscles in the small bronchi. Conclusions: In COPD, the capability of inflammatory cells to produce certain AA metabolites was decreased after inhaled FP treatment This result is discussed in its relation to clinical effects, the influence of smoking, and the results of an earlier, similar study in asthma patients
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