TY - JOUR T1 - Reduced phagocytosis of pathogenic bacteria by neutrophils from COPD patients JF - European Respiratory Journal JO - Eur Respir J VL - 40 IS - Suppl 56 SP - 387 AU - Catherine Thomas AU - Peter Barnes AU - Louise Donnelly Y1 - 2012/09/01 UR - http://erj.ersjournals.com/content/40/Suppl_56/387.abstract N2 - Acute exacerbations of COPD are the commonest cause of acute medical admissions in the UK, with ∼50% associated with bacterial infection. An acute bacterial insult is usually associated with increased recruitment and activation of neutrophils. COPD is characterized by airway neutrophilia; however, despite increased numbers of these cells, bacterial colonization persists. This study examined whether neutrophil phagocytosis was altered in COPD. Neutrophils were obtained from COPD, smoking and healthy subjects and phagocytosis of fluorescently-labelled polystyrene beads, Haemophilus influenzae (HI) or Streptococcus pneumoniae (SP) measured by flow cytometry. Neutrophils from all subjects ingested beads similarly showing that all cells were capable of phagocytosis. Neutrophils from all subjects phagocytosed SP with a maximum response at 5 min, however COPD neutrophils ingested significantly less SP (p<0.05) than those isolated from non-smokers (NS) and smokers (S) (NS: 17.1 ± 1.7 MFI, n=19 vs S: 14.8 ± 1.2 MFI, n=19 vs COPD: 12.8 ± 0.5 MFI, n=20). Approximately 95% of cells phagocytosed HI, but the capacity of COPD neutrophils to ingest HI was significantly attenuated (p<0.01) compared with control neutrophils for all time points up to 30 min. Neutrophils from S phagocytosed HI similarly to cells from NS initially (NS: 18.0 ± 3.8 MFI, n=19 vs S: 19.3 ± 4.8 MFI, n=20 vs COPD: 5.2 ± 1.5 MFI, n=20). However, after 10 min this response became blunted. These effects were not associated with differences in expression of CD11b, TLR2 or TLR4 or in cell viability. Therefore, neutrophils from COPD patients exhibit reduced phagocytosis of pathogenic bacteria which could account for persistent airway colonization. ER -