Background and Objective. Chronic obstructive pulmonary disease (COPD) is characterized by a persistence of inflammation in large and small airways. We hypothesized that this could be caused by the inability of an inflammatory process to resolve. In the resolution of inflammation, a switching of arachidonic acid metabolism from the production of proinflammatory leukotriene B4 (LtB4) to the synthesis of anti-inflammatory lipoxins plays an important role. The aim of our study was to determine the content of lipoxin A4 (LXA4) and LtB4 in induced sputum of patients with exacerbated COPD and to compare it to healthy controls, as well as to analyze the relationship between proinflammatory and anti-inflammatory mediators and an inflammatory cell spectrum in induced sputum. Material and Methods. Induced sputum from 17 COPD patients and 7 healthy controls were analyzed for LXA4 and LtB4 content and inflammatory cell spectrum. Results. COPD patients had a significantly lower sputum LXA4 concentration and LtB4/LXA4 ratio compared with healthy controls. A significant negative correlation was found between the LXA4 concentration and the relative neutrophil count and between the LtB4/LXA4 ratio and the relative macrophage count. Conclusions. COPD patients during the late phase of exacerbation had a suppressed production of LXA4 and an elevated LtB4/LXA4 ratio in induced sputum demonstrating a proinflammatory imbalance. The correction of a balance between proinflammatory and anti-inflammatory eicosanoids by the administration of stable analogues of lipoxins could improve the treatment of chronic obstructive pulmonary disease in the future.

This study demonstrates that young smokers have early inflammatory changes in their airways that not only initiate nonspecific mechanisms recruiting neutrophils, but also involve specific immune mechanisms with recruitment of T regulatory lymphocytes. The lymphocyte response is probably adaptive.