DEFB4A and chronic obstructive pulmonary disease: Our study adds to this information by showing that exposure of differentiated primary airway epithelial to whole DE, instead of aged DE particles in suspension, decreases NTHI-induced expression of DEFB4A/hBD2 and S100A7. Although this inhibition did not reach statistical significance due to substantial inter-donor variation, a DE-induced impairment of expression of these and other antimicrobial peptides may be highly relevant to COPD considering the strong link between both exposure to particulate air pollution and COPD exacerbations [7–9], and between NTHi and COPD exacerbations [10].