Increased uptake of<i>haemophilus influenzae</i>by primary airway epithelial cells from COPD patients

<b>Rationale:</b> Most hospitalizations in the UK are due to exacerbations of chronic obstructive pulmonary disease (COPD), but why some patients are prone to recurring exacerbations is unclear. One reason could be recolonisation of the airways by bacteria that hide in airway epithelial cells following antibiotic treatment. To test this, airway epithelial cells from non-smokers and COPD patients were exposed to fluorescently labelled <i>Haemophilus influenzae</i> and uptake measured. <b>Methods:</b> Primary airway epithelial cells from both non-smokers (n=5) and COPD patients (n=5) were exposed to fluorescently labelled heat-killed <i>H. influenzae</i> for 72h. Extra-cellular fluorescence was quenched using Trypan blue and internal fluorescence measured fluorimetrically. Cell viability was measured by MTT assay. <b>Results:</b> Airway epithelial cells ingested <i>H. influenzae</i> in a time-dependent manner up to 72h without causing cell death. However, airway epithelial cells from COPD patients ingested more bacteria than cells obtained from healthy controls (Fig. 1). <b>Conclusion:</b> COPD epithelial cells appear to have increased capacity to engulf <i>H. influenzae</i> compared with healthy cells, implying that following antibiotics, bacteria stored within these cells may be released and recolonize the airways leading to subsequent exacerbations. Targeting this mechanism in the airway epithelium may prevent repeat exacerbations in the future.