Adhesion molecules in subjects with COPD and healthy non-smokers: a cross sectional parallel group study

Abstract

BackgroundThe aim of the study was to investigate how the expression of adhesion molecules changes as neutrophils migrate from the circulation to the lung and if these changes differ between non-smoking subjects and smokers with and without COPD.MethodsNon-smoking healthy subjects (n=22), smokers without (n=21) and with COPD (n=18) were included. Neutrophils from peripheral blood, sputum and bronchial biopsies were analysed for cell surface expression of adhesion molecules (CD11b, CD62L, CD162). Serum, sputum supernatant and BAL-fluid were analysed for soluble adhesion molecules (ICAM-1, -3, E-selectin, P-selectin, VCAM-1, PECAM-1).ResultsExpression of CD11b was increased on circulating neutrophils from smokers with COPD. It was also increased on sputum neutrophils in both smokers groups, but not in non-smokers, as compared to circulating neutrophils.Serum ICAM-1 was higher in the COPD group compared to the other two groups (p<0.05) and PECAM-1 was lower in smokers without COPD than in non-smoking controls and the COPD group (p<0.05). In BAL-fluid ICAM-1 was lower in the COPD group than in the other groups (p<0.05).ConclusionsThus, our data strongly support the involvement of a systemic component in COPD and demonstrate that in smokers neutrophils are activated to a greater extent at the point of transition from the circulation into the lungs than in non-smokers.

Intercellular adhesion molecule 1 and progression of percent emphysema: The MESA Lung Study

“…These findings are consistent with small studies showing that circulating sICAM-1 is increased in patients with COPD (11, 12). The result for sE-selectin was of similar magnitude to sICAM-1 in minimally adjusted analyses, but was non-significant, in part due to the smaller sample size, and was further attenuated after full adjustment.…”

“…ICAM-1 blocking antibodies reduce neutrophilic pulmonary inflammation by two-thirds in animals, suggesting that ICAM-1 may be critical in neutrophil access to the lung (10). Small studies have found altered ICAM-1 and E-selectin in COPD (11, 12), and cross-sectional studies have found inverse associations between soluble ICAM-1 (sICAM-1) and lung function (13, 14). However, no longitudinal study has assessed the relationship between ICAM-1 or E-selectin and the progression of emphysema or decline in lung function.…”

Investigation of blood neutrophil structural and functional characteristics in patients with chronic obstructive pulmonary disease and pulmonary hypertension using atomic force microscopy

“…В ряде исследований показано, что увеличение плазменных растворимых молекул межклеточной адгезии ICAM 1 оказывает повреждающее действие на эндотелий [20]. K.Blidberg et al установлено, что уровни растворимого ICAM 1, ICAM 3 в сыворотке увеличивается при ХОБЛ, что подтверждает систем ную воспалительную активность [5].…”

“…Согласно резуль татам многочисленных исследований, у больных ХОБЛ отмечаются изменения структуры и актива ция одних из основных эффекторных клеток -нейт рофилов периферической крови [3]. У больных ХОБЛ нейтрофилами секретируются сериновые про теазы, включая нейтрофильную эластазу, катепсин G и протеиназу 3, которые приводят к деструкции аль веолярной стенки, обладают повышенной хемотак сической реакцией и экспрессией поверхностных клеточных адгезивных молекул [4], что свидетель ствует о системной воспалительной активности [5].…”

Reasonability and perspectives of anti-cytokine and immune correcting therapy in patients with chronic obstructive pulmonary disease

“…Эта молекула экспрессируется клетками крови (тромбоцитами, нейтрофилами, моноцитами, лимфоцитами) и эндо телиальными клетками. Концентрация растворимой формы PECAM 1 в сыворотке крови курящих паци ентов с ХОБЛ выше, чем у курящих здоровых лю дей [48]. Кроме того, у курящих пациентов с ХОБЛ повышено количество циркулирующих в крови эн дотелиальных микрочастиц, содержащих PECAM 1, по сравнению с курящими здоровыми людьми.…”