Introduction Vitamin D binding protein (DBP) plays a role in macrophage activation and neutrophil chemotaxis, both functions being relevant to COPD and airway infection. We have shown previously that DBP is present in the COPD lung and relates directly to macrophage activation.1 Transcription of DBP is stimulated by inflammatory cytokines,2 which tend to be raised in exacerbations. DBP is also cleaved from its binding site on neutrophils by the action of neutrophil elastase.3 We reasoned that DBP would be elevated in the lung and systemic circulation during exacerbations of COPD compared to the stable state.
Methods 20 patients with a known diagnosis of COPD were studied in the stable state and at the start of an exacerbation. Circulating CRP, elastase, AAT and DBP were measured at each time point, together with sol phase DBP, AAT and CRP, where sufficient sample was available (n=9). All clinical parameters were studied in the stable state only. Relationships between exacerbation and stable state were sought using pair-wise tests for each individual, whilst group relationships between DBP, CRP and elastase were sought using Spearman's rank correlation.
Results No significant differences between stable state and exacerbation were seen for circulating or sol phase DBP (both p>0.4). Circulating CRP and AAT were significantly higher in exacerbation (mean difference 3.95, p<0.0001 and 137.39, p=0.03 respectively), as were sol phase CRP and AAT (mean difference 18.29, p=0.003 and 0.60, p=0.009 respectively). DBP did not relate to elastase in either stable state (p=0.61) or exacerbation (p=0.17), nor to CRP (p=0.71 and 0.98, respectively).
Conclusions The level of local and systemic inflammation, with consequent elastase release, during a COPD exacerbation is insufficient to alter DBP levels. As such it is unlikely that DBP-derived macrophage activation is important in their pathogenesis or resolution.