Pro-inflammatory potential of wood smoke and traffic-derived particles in a monocytic cell line.
Lung inflammation is an important process in host defence to inhaled particulate matter. To what extent physicochemical properties of particles from different sources influence their inflammatory potential has not been fully clarified. The aim of this study was to investigate the potential of particles from wood smoke and traffic to induce a release of pro-inflammatory cytokines in the monocytic cell line THP-1. The influence of endotoxin on cytokine release was investigated using the inhibitor polymyxin B sulphate, whereas the responses to native particles, washed particles and their organic extracts were compared to determine the role of the organic fraction. Particles from the two sources showed a similar inflammatory potential, but the response was mediated by different particle characteristics. The organic fraction of wood smoke accounted for the majority of the cytokine release, whereas the response to the traffic-derived particles was in addition influenced by endotoxin and the particle core. The sum of the cytokine release induced by the organic extract and washed particles was lower than that induced by native particles, suggesting that the organic fraction must be adsorbed to the particles to exert biological activity. The results also indicated that different particle characteristics may activate different signalling pathways, since inhibition of endotoxin reduced release of TNF-alpha, IL-1beta and IL-8, whereas organic extraction only affected release of TNF-alpha and IL-8. Together, these data illustrate that a similar inflammatory response may be mediated by different particle characteristics and possibly through different signalling pathways.
Kocbach
Anette
A
Division of Environmental Medicine, Norwegian Institute of Public Health, P.O. Box 4404, Nydalen, 0403 Oslo, Norway. Anette.Kocbach@fhi.no
Namork
Ellen
E
Schwarze
Per E
PE
D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology; D052638:Particulate Matter / Q000009:adverse effects*; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity; D012333:RNA, Messenger / Q000032:analysis; D012906:Smoke / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D001335:Vehicle Emissions / Q000633:toxicity; D014934:Wood / Q000009:adverse effects*
D016207:Cytokines; D053583:Interleukin-1beta; D016209:Interleukin-8; D008070:Lipopolysaccharides; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons; D012333:RNA, Messenger; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D001335:Vehicle Emissions