PT - JOURNAL ARTICLE AU - Richa Singh AU - Kylie Belchamber AU - Alexander Mackay AU - Beverly Kowlessar AU - James Allinson AU - Simon Brill AU - Gavin Donaldson AU - Peter Barnes AU - Jadwiga Wedzicha AU - Louise Donnelly TI - TNFα release by monocyte-derived macrophages at stable and exacerbation states in COPD DP - 2014 Sep 01 TA - European Respiratory Journal PG - 2957 VI - 44 IP - Suppl 58 4099 - http://erj.ersjournals.com/content/44/Suppl_58/2957.short 4100 - http://erj.ersjournals.com/content/44/Suppl_58/2957.full SO - Eur Respir J2014 Sep 01; 44 AB - Inflammation is a hallmark of COPD and contributes to its pathogenesis. Inflammatory cells, such as alveolar macrophages, release inflammatory mediators including TNFα. We investigated basal and bacteria stimulated TNFα release by monocyte-derived macrophages (MDMs) at stable and exacerbation states.MDMs were cultured from 26 COPD patients at paired stable and exacerbation states. The MDMs were incubated for 4 h at 37oC with 100μl of RPMI (controls), inert beads (4.5x109 microspheres/ml), or heat-killed Haemophilus influenzae (HI) or Streptococcus pneumoniae (SP) (both at 5x108 cfu/ml). Subsequent TNFα release was measured by ELISA.There was no difference in basal TNFα release from MDMs at stable and exacerbation states (p=0.247). There was a significant difference in TNFα release between the inert beads, HI and SP (p<0.001), with higher TNFα release in response to HI compared to SP irrespective of patient state (p<0.05). Inert beads did not stimulate TNFα release (p>0.05). In response to SP, TNFα release significantly increased at exacerbation compared to stable state (p=0.007, Figure 1A), but not in response to HI (p=0.513, Figure 1B).HI is more pro-inflammatory than SP at both stable and exacerbation COPD states. However, a significant increase in TNFα release from stable to exacerbation state is only seen in response to SP. Further work is needed to investigate this response and the relationship with phagocytosis.