Abstract
BACKGROUND: Non-typeable haemophilus influenzae (NTHi) is the most common bacteria present in the airways of patients with neutrophilic COPD, and is found persistently in 30% of patients and in 50% during exacerbation. Neutrophilic patients with COPD do not respond to inhaled corticosteroid treatment. We examine how budesonide, fluticasone propionate and dexamethasone affect the inflammatory response of bronchial epithelial cells upon NTHi challenge.
METHODS: Human bronchial epithelial cells from three healthy non-smoking donors were grown to 90% confluence at passage 3 in Bronchial Epithelial Growth Media (Lonza). These cells were treated with 16nM and 1.6nM budesonide, 10nM and 1nM fluticasone propionate or 100nM and 10nM dexamethasone for two hours prior to addition of ∼1x106 CFU of NTHi. Cultures were incubated for a further hour before supernatants were collected and tested for IL-8 concentration by ELISA (R&D Systems).
RESULTS: Basal release of IL-8 was four fold lower than that upon stimulation with NTHi (mean: 165.9pg/ml, SD: 202.9 compared to 693.5pg/ml, SD: 83.09). Budesonide, fluticasone propionate and dexamethasone decrease the level of IL-8 released from the epithelial cells in a concentration-dependant manner, however did not reach significance (high concentrations: p=0.095, p=0.071 and p=0.095 respectively).
CONCLUSION: IL-8 release shows a trend to being dampened by corticosteroid treatment, however do not return to basal levels. This may in part be responsible for the higher neutrophil count associated with those COPD patients with persistent NTHi infection.
- Copyright ©the authors 2016