Differential responses of COPD macrophages to respiratory bacterial pathogens.

COPD patients have increased susceptibility to airway bacterial colonisation. and are three of the most common respiratory bacterial species in COPD. colonisation but not other bacteria, in COPD patients is associated with higher sputum neutrophil counts. Alveolar macrophages are key in clearance of bacteria as well as releasing mediators to recruit and activate other immune cells in response to infection. The aim was to characterise differences in COPD macrophage responses to focusing on release of inflammatory and chemotactic mediators, and apoptosis regulation.  Lung macrophages and monocyte-derived macrophages from COPD patients and control subjects were exposed to Cytokine secretion tumour necrosis factor interleukin (IL)-6, CXCL8, CCL5 and IL-1β) were measured by ELISA and quantitative reverse transcriptase PCR (RT-qPCR), and apoptosis genes MCL-1, BCL-2, BAX and BAK1 by RT-qPCR. Apoptosis and reactive oxygen species (ROS) release were also measured.  Macrophages responded differentially to the bacterial species, with increased, prolonged production of the neutrophil chemoattractant CXCL8 in response to and but not . initiated macrophage apoptosis and ROS release, and did not and increased anti-apoptosis gene expression (BCL-2 5.5-fold and MCL-1 2.4-fold, respectively).  Differential cytokine responses of macrophages to these bacterial species can explain neutrophilic airway inflammation associated with but not in COPD. Furthermore, delayed macrophage apoptosis is a potential mechanism contributing to inability to clear .