Identification of novel pathogenic mechanisms triggered by arginase activation in patients with COPD

Introduction: The advancement in the pathophysiology of COPD regarding inflammation has led to new questions and research lines.Our objectives were to establish new pathogenic mechanisms of COPD in stable and exacerbated phases, through inflammation and immunosuppression, and describe the role of arginase in these phases. Patients and Methods: Prospective and case control study with three groups: healthy subjects (15), COPD in stable phase (18) and COPD in exacerbated phase (14). This last one was reassessed 3 months later in stable phase and were included in the COPD stable group (total number: 32). Biometrical data, respiratory function and blood analytical data were obtained. Arginase activity in serum, total lymphocyte subpopulations count and CD3z expression were measured. Results: There were no differences between control group and stable COPD group regarding arginase activity but CD3z expression was lower in stable COPD group (p 0.081) Regarding control and exacerbated COPD group, arginase activity was higher in exacerbated COPD group (p 0.039). CD3z expression, CD3, CD4 and NK-CD56++ count were lower in the exacerbated COPD group (p Arginase activity was higher in exacerbated COPD group compared to stable COPD group (p 0.110). CD3z expression, CD3, CD4, CD8 and NK-CD56++ count were lower in exacerbated COPD group (p Conclusion: A trend towards higher values of arginase activity and lower CD3z expression was noted in COPD patients in stable and exacerbated phases.