Introduction COPD exacerbations are the main cause of hospital admission and death in COPD. Respiratory viruses are identified in over half COPD exacerbations with human rhinovirus (HRV) being the most commonly detected. Secondary bacterial infection is associated with prolonged exacerbations, higher rates of hospital admission and increased symptom severity. Our group have previously shown that secondary bacterial infection in HRV induced COPD exacerbations is driven by an outgrowth of Haemophilus influenzae.

Hypothesis We hypothesised that HRV may impair phagocytosis of bacteria by alveolar macrophages which may lead to secondary bacterial outgrowth in COPD exacerbations.

Methods Bronchoscopy was performed on participants of the London COPD cohort and healthy controls. Alveolar macrophages were obtained by bronchoalveolar lavage. Alveolar macrophages were incubated with HRV at a multiplicity of infection (MOI) of 5 for 24 hours or media control. Phagocytic capacity was assessed by incubating with fluorescently labelled heat killed Haemophilus influenzae or Streptococcus pneumoniae for 4 hours. Uptake was measured in Relative Fluorescent Units (RFU) using a fluorimeter.

Results Alveolar macrophages were obtained from 14 COPD patients and 9 healthy controls. HRV significantly impaired phagocytosis of H. influenzae by alveolar macrophages in patients with COPD (HRV median 0.97 (0.50–2.17 interquartile range) RFU x10³ vs media control median 1.38 (0.70–2.50 interquartile range) RFU x10³ p<0.05) but did not impair phagocytosis of S. pneumoniae. HRV did not impair phagocytosis in alveolar macrophages from healthy controls. Baseline phagocytic capacity of H. influenzae was impaired in COPD patients compared to healthy controls (COPD 1.59+/-1.31 RFU x10³ vs healthy control 3.81+/-1.82 RFU x10³). Phagocytosis of H. influenzae correlated with worsening FEV1 percent predicted in COPD (R²=0.452 p<0.05).

Conclusions The presence of HRV impaired phagocytosis of H. influenzae in alveolar macrophages from patients with COPD but not healthy controls. This may contribute to secondary bacterial infection in COPD exacerbations.