RT Journal Article
SR Electronic
T1 Lipoxin A4 receptor expression in smokers with and without COPD
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP p3900
VO 38
IS Suppl 55
A1 Liga Balode
A1 Sergejs Isajevs
A1 Darja Svirina
A1 Uldis Kopeika
A1 Gunta Strazda
A1 Immanuels Taivans
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/p3900.abstract
AB Background: The lipoxin A4 receptor, LXA4R/FPRL-1, is a G protein-coupled receptor. LXA4R with high affinity binds anti-inflammatory lipoxin LXA4 and with low affinity - N-formylated proinflammatory peptides. The aim of our study was to evaluate FPRL-1 expression in nonsmokers, asymptomatic smokers and in patients with COPD.Patients and methods: 6 nonsmokers, 7 asymptomatic smokers and 5 moderate COPD patients undergoing lung resection for a solitary peripheral non-small cell carcinoma were enrolled in the study. Immunohistochemical methods were used to evaluate FPRL expression in airways and alveolar walls.Results: FPRL-1 expression was observed in airways epithelial cells, macrophages, lymphocytes and neutrophils. Obtained results showed that asymptomatic smokers had increased numbers of FPRL-1 positive cells in alveolar walls compared to nonsmokers (157±59 vs 38±13 cells/mm2, p= 0.002). At contrast, COPD patients had decreased numbers of FPRL-1 positive cells compared to asymptomatic smokers (23±7 vs 157±59 cells/mm2, p= 0.002). In addition, COPD patients had a tendency of decreased FPRL-1 expression compared to nonsmokers. When all smokers were analyzed together, a significant positive correlation was found between the number of FPRL positive cells and airflow obstruction, FEV1% (Rho=+0.66, p=0.02).Conclusion: Downregulated FPRL-1 in COPD patients may explain persistence of inflammatory process in alveolar area in COPD, whereas upregulation in asymptomatic smokers could serve as adaptive mechanism limiting inflammatory process.