Biomass smoke particles induce cytokines and reduce phagocytosis by monocyte-derived macrophages

In industrialised nations, cigarette smoking is the major risk factor for COPD, but in the developing world, exposure to biomass smoke (BMS) particles accounts for ∼50% of COPD deaths. COPD is associated with an increase in macrophages, albeit functionally defective. We hypothesise that exposure to BMS particles will elicit an inflammatory response and decrease phagocytosis of bacteria by monocyte derived macrophages (MDM). BMS particles were collected from a rural kitchen in India by burning wood and animal dung in a standard 3-stone cookstove using a high volume sampler. MDM from non-smoker (NS n=2-4) and COPD (n=2-5) subjects were exposed to BMS (1-300μg/ml) ± polymyxin B (10μg/ml) for 24h to eliminate LPS contamination. MDM were then incubated for 4h with fluorescently labelled heat killed H. influenzae (HI), S. pneumoniae (SP) or inert beads. Phagocytosis was measured by fluorimetry, cytokine release by ELISA and viability by MTT. BMS particles caused a concentration-dependent increase in CXCL8 (max release NS: 54±13.8 ng/ml; COPD: 42±1.1ng/ml) and IL-6 (max release NS: 6.2±0.7ng/ml; COPD: 7.3±3.3ng/ml) and TNFα (max release NS: 1.5±0.5ng/ml, COPD no stim). BMS particles stimulated release of IL-10 from COPD MDM (0.3±0.1ng/ml) but not from NS MDM. Polymyxin B had minimal effect on BMS particle-induced cytokine release. BMS particles had no effect on phagocytosis of HI, SP or beads by MDM from NS subjects. However, BMS particles reduced phagocytosis of HI by 55.1±2.7% and SP by 36.9±28.1% by COPD MDM. Viability was not affected. BMS particles are pro-inflammatory independent of LPS contamination and may drive defective macrophage phagocytosis in COPD.