Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B-4

Citation
Sw. Crooks et al., Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B-4, EUR RESP J, 15(2), 2000, pp. 274-280
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
EUROPEAN RESPIRATORY JOURNAL
ISSN journal
09031936 → ACNP
Volume
15
Issue
2
Year of publication
2000
Pages
274 - 280
Database
ISI
SICI code
0903-1936(200002)15:2<274:BIIABE>2.0.ZU;2-D
Abstract
Neutrophils recruited to the airways in chronic obstructive pulmonary disea se (COPD) are thought to mediate tissue destruction. Neutrophil recruitment is increased during bacterial exacerbations. The inflammatory process was studied in patients with an acute exacerbation of COPD in order to ascertai n the role of leukotriene B-4 (LTB4). The sputum of eight subjects with a bacterial exacerbation of COPD was anal ysed for neutrophil products (myeloperoxidase, elastase) and chemoattractan ts (interleukin-8 (IL-8) and LTB4). The contribution of LTB4 to the chemota ctic activity of the sputum sol phase was determined using the LTB4 recepto r antagonist LY293111. The concentrations of the serum acute phase proteins alpha(1)-proteinase inhibitor, alpha(1)-antichy-motrypsin and C-reactive p rotein were measured. All patients received appropriate broad-spectrum anti biotic treatment for 7-14 days. Initially, the sputum myeloperoxidase activity was high, indicating neutrop hil influx; this was associated with high levels of IL-8 and LTB4. All thes e concentrations fell with treatment (p<0.01). The chemotactic activity of the sputum was raised on presentation and fell with treatment (p<0.01). LTB 4 contributed similar to 30% of the total chemotactic activity on presentat ion; this diminished with therapy. All acute phase proteins were raised on presentation and fell with therapy (p<0.01). These findings suggest that leukotriene B-4 contributes to neutrophil influ x into the airway in chronic obstructive pulmonary disease and may influenc e disease progression.