Search

Identification of biomarkers for the novel therapeutics targets of Chronic obstructive pulmonary disease (COPD) is an important area of current research. In this study, the level of inflammatory cytokines was investigated and correlated these levels with erythrocytic antioxidant activities in COPD patients with smokers and without smokers and parameters of severity.Plasma levels of Interleukin (IL)-6, IL-8 and IL-10 concentrations were assayed by means of Enzyme-linked Immunosorbent Assay (ELISA) and erythrocytic glutathione-s-transferase (GST) and glutathione peroxidase (GPx) activities were estimated by spectrophotometric method.Both IL-6 and IL-8 plasma levels showed a statistically significantly higher in COPD patients as compared to healthy controls (p0.05) and GPx activities (r= - 0.080, p>0.05). Similarly IL-8 was also found negative association with GST (r= - 0.260, p>0.05) and GPx activities (r= - 0.268, p>0.05). Whereas, a significant positive association was observed between IL-10 and erythrocytic GST (r= 0.494, p In conclusion, Plasma levels of inflammatory cytokines IL-6 and IL-8 are related with severity of COPD and IL-10 and oxidative stress markers GST and GPx are co-dependent and strongly interrelated processes and may be used as a potential marker for the evaluation of COPD.

ICAM-1 is required for firm adhesion of leukocytes to the endothelium. However, how the spatial organization of endothelial ICAM-1 regulates leukocyte adhesion is not well understood. In this study, we identified the calcium-effector protein annexin A2 as a novel binding partner for ICAM-1. ICAM-1 clustering promotes the ICAM-1–annexin A2 interaction and induces translocation of ICAM-1 into caveolin-1–rich membrane domains. Depletion of endothelial annexin A2 using RNA interference enhances ICAM-1 membrane mobility and prevents the translocation of ICAM-1 into caveolin-1–rich membrane domains. Surprisingly, this results in increased neutrophil adhesion and transendothelial migration under flow conditions and reduced crawling time, velocity, and lateral migration distance of neutrophils on the endothelium. In conclusion, our data show that annexin A2 limits neutrophil transendothelial migration by organizing the spatial distribution of ICAM-1.