RT Journal Article SR Electronic T1 Enhanced IL-6 and CCL3 activity in COPD JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP P791 VO 40 IS Suppl 56 A1 Arjun Ravi A1 Shruti Khurana A1 Jonathan Plumb A1 George Booth A1 Matthew Catley A1 Emma Smith A1 Louise Healy A1 Jørgen Vestbo A1 Dave Singh YR 2012 UL http://erj.ersjournals.com/content/40/Suppl_56/P791.abstract AB RationaleIL-6 is a pleiotropic cytokine that is involved in the regulation of inflammation. Increased serum IL-6 levels are associated with reduced FEV1 in COPD patients independent of age or smoking status. Elevated levels of sputum IL-6 in COPD patients have been associated with increased exacerbation frequency. The mechanism by which IL-6 may mediate inflammation in COPD is uncertain. We sought to determine levels of IL-6 and its soluble receptor (sIL-6R) in COPD sputum. IL-6 signaling can alter the levels of the neutrophil chemoattractant CCL3 and the monocyte chemoattractant CCL2; we also investigated the levels of these chemokines.Methods70 patients with GOLD stage I-IV COPD and 30 healthy controls comprising of 15 healthy smokers (HS) and 15 healthy non-smokers (HNS) underwent sputum sampling with PBS processing. Levels of IL-6, sIL-6R, CCL2, CCL3 were determined by multiplex analysis (MSD® platform) of sputum supernatant.ResultsHealthy smokers expressed the highest levels of sputum IL-6. COPD patients expressed the highest levels of sIL-6R. COPD patients also expressed the highest levels of sputum CCL3. In contrast, CCL2 expression was significantly reduced in COPD patients.View this table:ConclusionWe report evidence of enhanced IL-6 signaling and CCL3 activity in COPD sputum. We have observed that there is reduced CCL2 activity and enhanced CCL3 activity in COPD sputum. IL-6 may therefore promote neutrophillic inflammation in COPD through up-regulation of CCL3 expression.