SWCNT suppress inflammatory mediator responses in human lung epithelium in vitro.
Single-walled carbon nanotubes have gained enormous popularity due to a variety of potential applications which will ultimately lead to increased human and environmental exposure to these nanoparticles. This study was carried out in order to evaluate the inflammatory response of immortalised and primary human lung epithelial cells (A549 and NHBE) to single-walled carbon nanotube samples (SWCNT). Special focus was placed on the mediating role of lung surfactant on particle toxicity. The toxicity of SWCNT dispersed in cell culture medium was compared to that of nanotubes dispersed in dipalmitoylphosphatidylcholine (DPPC, the main component of lung lining fluid). Exposure was carried out for 6 to 48 h with the latter time-point showing the most significant responses. Moreover, exposure was performed in the presence of the pro-inflammatory stimulus tumour necrosis factor-alpha (TNF-alpha) in order to mimic exposure of stimulated cells, as would occur during infection. Endpoints evaluated included cell viability, proliferation and the analysis of inflammatory mediators such as interleukin (IL)-8, IL-6, TNF-alpha and macrophage chemoattractant protein-1 (MCP-1). Crocidolite asbestos was included as a well characterised, toxic fibre control. The results of this study showed that HiPco SWCNT samples suppress inflammatory responses of A549 and NHBE cells. This was also true for TNF-alpha stimulated cells. The use of DPPC improved the degree of SWCNT dispersion in A549 medium and in turn, leads to increased particle toxicity, however, it was not shown to modify NHBE cell responses.
Herzog
Eva
E
Radiation and Environmental Science Centre (RESC), Focas Institute, Dublin Institute of Technology, Kevin Street, Dublin 8, Ireland. eva.herzog@dit.ie
Byrne
Hugh J
HJ
Casey
Alan
A
Davoren
Maria
M
Lenz
Anke-Gabriele
AG
Maier
Konrad L
KL
Duschl
Albert
A
Oostingh
Gertie Janneke
GJ
D015060:1,2-Dipalmitoylphosphatidylcholine / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000633:toxicity*; D017638:Asbestos, Crocidolite / Q000633:toxicity*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D037742:Nanotubes, Carbon / Q000633:toxicity*; D011401:Promoter Regions, Genetic / Q000187:drug effects; D037661:Pulmonary Surfactant-Associated Proteins / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018836:Inflammation Mediators; D037742:Nanotubes, Carbon; D037661:Pulmonary Surfactant-Associated Proteins; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D017638:Asbestos, Crocidolite; D015060:1,2-Dipalmitoylphosphatidylcholine