S131 Human macrophage model of biomass smoke exposure shows impaired ingestion of Streptococcus pneumoniae
Background Three billion people worldwide, primarily in less economically developed countries use biomass fuel (BMF) as their main source of household energy. In children, the risk of pneumonia is increased by exposure to BMF smoke by a factor of 1.8. In adults, an epidemiological association between acute pneumonia and outdoor air pollution and tobacco smoke exposure has been demonstrated but there are no data confirming an association between pneumonia and BMF smoke exposure. Few mechanistic studies have been performed in humans investigating the association between BMF exposure and S pneumoniae. This work aimed to assess the phagocytic ability of particulate matter (PM) challenged macrophages on fluorescent labelled beads and S pneumoniae.
Methods In order to model BMF exposure, monocyte derived macrophages (MDMs), from 12 day old buffy coats, were challenged with different types and doses of PM (fine carbon black (FCB), Malawi wood and Norwegian wood). The percentage area of the macrophage cytoplasm that PM occupied (PM load) was calculated using image analysis software (Image SXM). The ability of PM challenged MDMs to phagocytose fluorescent labelled beads and S pneumoniae was assessed by counting the beads / bacteria associated with MDMs, using fluorescent microscopy.
Results Increasing the PM dose was associated with a decrease in the percentage of cells associated with S pneumoniae (Abstract S131 figure 1A) and beads. The same result was observed when the average number of S pneumoniae (or beads) within cells was used as the outcome measure. With all three PMs used, a lower PM load was correlated with a higher capacity to phagocytose S pneumoniae and beads. Malawi wood and Norwegian wood impaired MDMs phagocytic ability more than FCB (Abstract S131 figure 1B).
Conclusions Our data demonstrate that MDMs exposed to PM have impaired ability to phagocytose beads and S pneumoniae and that wood smoke exposed MDMs had a greater phagocytic impairment than FCB. These observations support an association between BMF smoke exposure and pneumonia. Our model enables further work to be carried out on the dose-response of smoke exposure and pneumococcal disease as well as into the pathogenesis of increased susceptibility to pneumococcal infection in BMF exposed individuals.