title: Particles from wood smoke and traffic induce differential pro-inflammatory response patterns in co-cultures.
abstract: The inflammatory potential of particles from wood smoke and traffic has not been well elucidated. In this study, a contact co-culture of monocytes and pneumocytes was exposed to 10-40 microg/cm(2) of particles from wood smoke and traffic for 12, 40 and 64 h to determine their influence on pro-inflammatory cytokine release (TNF-alpha, IL-1, IL-6, IL-8) and viability. To investigate the role of organic constituents in cytokine release the response to particles, their organic extracts and the washed particles were compared. Antagonists were used to investigate source-dependent differences in intercellular signalling (TNF-alpha, IL-1). The cytotoxicity was low after exposure to particles from both sources. However, wood smoke, and to a lesser degree traffic-derived particles, induced a reduction in cell number, which was associated with the organic fraction. The release of pro-inflammatory cytokines was similar for both sources after 12 h, but traffic induced a greater release than wood smoke particles with increasing exposure time. The organic fraction accounted for the majority of the cytokine release induced by wood smoke, whereas the washed traffic particles induced a stronger response than the corresponding organic extract. TNF-alpha and IL-1 antagonists reduced the release of IL-8 induced by particles from both sources. In contrast, the IL-6 release was only reduced by the IL-1 antagonist during exposure to traffic-derived particles. In summary, particles from wood smoke and traffic induced differential pro-inflammatory response patterns with respect to cytokine release and cell number. Moreover, the influence of the organic particle fraction and intercellular signalling on the pro-inflammatory response seemed to be source-dependent.
authors.affiliation: Division of Environmental Medicine, Norwegian Institute of Public Health, Geitemyrsveien 75, 0462 Oslo, Norway. anette.kocbach@fhi.no
authors.forename: Anette
authors.initials: A
authors.lastname: Kocbach
authors.forename: Jan Inge
authors.initials: JI
authors.lastname: Herseth
authors.forename: Marit
authors.initials: M
authors.lastname: Låg
authors.forename: Magne
authors.initials: M
authors.lastname: Refsnes
authors.forename: Per E
authors.initials: PE
authors.lastname: Schwarze
mesh_terms: D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D018920:Coculture Techniques / Q000379:methods; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000633:toxicity*; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D012906:Smoke / Q000009:adverse effects*; D001335:Vehicle Emissions / Q000633:toxicity*; D014934:Wood / Q000032:analysis / Q000633:toxicity*
chemical_list: D018836:Inflammation Mediators; D052638:Particulate Matter; D012906:Smoke; D001335:Vehicle Emissions