Abstract
Introduction: Neutrophils of COPD patients are characterized by changes in activation of the respiratory burst. The aim of this study was to investigate the control of the respiratory burst in neutrophils of COPD patients upon engagement of the integrin Mac-1 (αM/β2; CD11b/CD18).
Methods: A cohort of 34 stable COPD patients (GOLD I-IV) was included in this study. Peripheral blood neutrophils were stimulated with formyl peptides (like fMLF) or anti-Mac-1 antibody (VIM12) and reactive oxygen species (ROS) production was measured by flow cytometry using Dihydrorhodamine 123 (DHR).
Results: The fMLF and anti-Mac-1 antibody (VIM12) induced ROS production in neutrophils from normal controls. Both fMLF and VIM12 were sensitive for priming by platelet-activating factor. The ROS production in neutrophils of COPD patients exhibited a primed phenotype in the context of fMLF. To our surprise the ROS production upon engagement of Mac-1 was markedly reduced in COPD patients compared to normal controls (332.8±64.7 vs. 876.8±275.7 respectively; p < 0.05). This was not associated with a lower expression of Mac-1 on the cell surface measured by flow cytometry.
Conclusion: Our data demonstrated the complex priming phenotype of neutrophils in COPD patients. The unresponsiveness of Mac-1 induced respiratory burst of neutrophils might indicate a shift towards a phenotype more sensitive for bacterial derived molecular patterns.
- © 2011 ERS
