PT - JOURNAL ARTICLE AU - Ekateina Makarova AU - Nikolay Menkov AU - Galina Varvarina AU - Monica Shoniya AU - Viktor Novikov TI - Influence of tobacco smoking on adhesion molecules profiles in patients with chronic obstructive lung disease DP - 2014 Sep 01 TA - European Respiratory Journal PG - P4194 VI - 44 IP - Suppl 58 4099 - http://erj.ersjournals.com/content/44/Suppl_58/P4194.short 4100 - http://erj.ersjournals.com/content/44/Suppl_58/P4194.full SO - Eur Respir J2014 Sep 01; 44 AB - Interactions between intercellular adhesion molecules (ICAM) and their ligands regulate leukocyte recruitment to inflammatory foci. Tobacco smoking dysregulates specific components of the adhesion cascade, which is pathogenic factor in smoking-induced diseases.Aim of the study: to investigate the influence of the smoking duration on the level of soluble (s) forms of ICAM and clinical features of chronic obstructive lung disease (COPD).Patients and methods: The levels of sICAM-1 (sCD54) and sICAM-3 (sCD50) were investigated in serum of 50 patients with COPD (14 females/36 males, mean age 60+10 years, mean FEV1 58,3+12%). The patients were divided in 2 groups: 1st group with smoking duration <30 pack-year (20 patients); 2nd group with smoking duration >30 pack-year (30 patients). Control group consisted of 30 healthy donors.Results: The frequency of COPD exacerbations and mMRC dyspnea index in patients with smoking duration >30 pack-years were significantly higher than in other group (mean exacerbation rate 2,3+0,5 and 1,3+0,7; mean mMRC index 3,4+1,2 and 2,5+1,1 respectively). The mean serum levels of sCD50 and sCD54 were significantly decreased in the 2nd group compared both with the 1st patient group and healthy donors. Correlations between smoking duration and serum sCD50 level (r=-0,43 p=0,04), as well as between FEV1 and sCD54 level (r=0,6, p=0,02) were observed.Conclusion. Severe course and frequent COPD exacerbations in patients with prolonged smoking duration was associated with decreased levels of sCD50 and sCD54 antigens suggesting the involving of cellular adhesion disturbances in COPD pathogenesis in heavy smokers.