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PKB has received project grant funding from GlaxoSmithKline. PJB has received project grant funding from GlaxoSmithKline and Astra-Zeneca. KFC has received project grant funding from GlaxoSmithKline and Pfizer. LED has received project grant funding Astra-Zeneca and Pfizer. The other authors have no competing interests.
ZL participated in the design of the study, carried out all assays on MDMs, performed the statistical analysis and drafted the manuscript. QZ participated in the design of the study, and performed assays on AMs. CMRT participated in the design of the study and generated labelled Haemophilus influenzae. KR performed assays on AMs. DG performed bronchoalveolar lavage on subjects for the AM study. PJB participated in the design and coordination of the study. LED participated in the design and coordination of the study and critically revised the manuscript. PKB and KFC conceived the study, participated in the design and coordination of the study and wrote the manuscript. All authors read and approved the final manuscript.
Bacteria are frequently cultured from sputum samples of severe asthma patients suggesting a defect in bacterial clearance from the airway. We measured the capacity of macrophages from patients with asthma to phagocytose bacteria.
Phagocytosis of fluorescently-labelled polystyrene beads, Haemophilus influenzae or Staphylococcus aureus by broncholaveolar lavage alveolar macrophages (AM) and by monocyte-derived macrophages (MDM) from non-asthmatics, mild-moderate and severe asthmatic patients was assessed using fluorimetry.
There were no differences in phagocytosis of polystyrene beads by AMs or MDMs from any of the subject groups. There was reduced phagocytosis of Haemophilus influenzae and Staphylococcus aureus in MDMs from patients with severe asthma compared to non-severe asthma (p < 0.05 and p < 0.01, respectively) and healthy subjects (p < 0.01and p < 0.001, respectively). Phagocytosis of Haemophilus influenzae and Staphylococcus aureus by AM was also reduced in severe asthma compared to normal subjects (p < 0.05). Dexamethasone and formoterol did not suppress phagocytosis of bacteria by MDMs from any of the groups.
Persistence of bacteria in the lower airways may result partly from a reduced phagocytic capacity of macrophages for bacteria. This may contribute to increased exacerbations, airway colonization and persistence of inflammation.