Modulation of airway inflammation in COPD
Inflammation in foregut derivatives outside the lung may contribute to amplification of airway inflammation. I have shown that a management strategy aiming to minimise eosinophilic airway inflammation as well as symptoms is associated with a significant 62% reduction in the frequency of severe exacerbations of COPD. This strategy was associated with no overall increase in corticosteroid treatment; there was evidence that increased corticosteroid therapy was targeted to patients with eosinophilic airway inflammation and benefit was largely confined to these patients. I have shown an association between the sputum differential neutrophil count and airway bacterial load, and showed that a one week course of Levofloxacin significantly reduced both the % neutrophil count and bacterial load in patients with stable state COPD and bacterial load > 106 cfu/ml. I have shown that the prevalence of peptic ulcer disease increases progressively with increasing severity of COPD in miners with homogeneous risk factors for development of COPD, and that peptic ulceration was a strong and independent predictor of a low FEV1 % predicted and FEV1/FVC ratio. In another population I showed that H.Pylori seropositivity was more common in patients with COPD compared to healthy smokers matched for age and occupation.;We have shown that TREM-1 can be measured from induced sputum and is potentially a novel marker of bacterial infection and neutrophilic airway inflammation during exacerbations.;Further work is required to ensure that measurement and modulation of airway inflammation results in improved clinical outcomes, and is made more clinically viable.