Levels changes of blood leukocytes and intracellular signalling pathways in COPD patients with respect to smoking attitude

• Published in: Clinical biochemistry 2008-04, Vol.41 (6), p.387-394
• Main Authors: Rumora, Lada, Milevoj, Lara, Popović-Grle, Sanja, Barišić, Karmela, Čepelak, Ivana, Grubišić, Tihana Žanić
• Format: Article
• Language: English
• Subjects: Aged; Bax; Bcl-2; COPD; Enzyme Activation; Humans; Leukocytes; Leukocytes - metabolism; Male; MAPK; Middle Aged; Mitogen-Activated Protein Kinases - metabolism; Oxidative stress; Pulmonary Disease, Chronic Obstructive - metabolism; Pulmonary Ventilation; Signal Transduction - physiology; Smoking
• ISSN: 0009-9120; 1873-2933
• DOI: 10.1016/j.clinbiochem.2007.12.013

To examine whether the proportions of blood leukocyte subsets are altered in COPD, and to assess the disturbances in signalling pathways in the leukocytes of COPD patients, with respect to smoking history. The study was performed at the Faculty of Pharmacy and Biochemistry and University Hospital for Lung Diseases, Zagreb, Croatia. Leukocyte counts were determined in 28 COPD male patients (11 smokers, 9 ex-smokers, 8 non-smokers) and 42 healthy male subjects (15 smokers, 13 ex-smokers, 14 non-smokers). We assessed activation of MAPKs (ERK, JNK, p38), and expression of Bcl-2 and Bax in the leukocytes by western blotting. Neutrophil and monocyte percentages were significantly increased, and lymphocyte percentage significantly decreased in COPD patients compared with healthy subjects ( p < 0.05). However, no significant smoking effect regarding leukocyte subsets was observed when compared current or former smokers with non-smokers of each studied group. ERK was activated in non-smokers only, especially in healthy ones. In contrast, strong induction of JNK and p38 phosphorylation, decreased Bcl-2 levels and increased Bax levels were detected in COPD smokers and COPD ex-smokers, but also in healthy individuals who smoke compared with healthy non-smokers ( p < 0.05). These results show that COPD and smoking affect intracellular signalling pathways. Understanding of the basic cellular and molecular mechanisms in COPD is essential for identification of molecules that may serve as targets for diagnosis and therapeutic interventions.