title: Pulmonary exposure to single-walled carbon nanotubes does not affect the early immune response against Toxoplasma gondii.
abstract: BACKGROUND
  Single-walled carbon nanotubes (SWCNT) trigger pronounced inflammation and fibrosis in the lungs of mice following administration via pharyngeal aspiration or inhalation. Human exposure to SWCNT in an occupational setting may occur in conjunction with infections and this could yield enhanced or suppressed responses to the offending agent. Here, we studied whether the sequential exposure to SWCNT via pharyngeal aspiration and infection of mice with the ubiquitous intracellular parasite Toxoplasma gondii would impact on the immune response of the host against the parasite.
  
  
  METHODS
  C57BL/6 mice were pre-exposed by pharyngeal administration of SWCNT (80 + 80 μg/mouse) for two consecutive days followed by intravenous injection with either 1x103 or 1x104 green fluorescence protein and luciferase-expressing T. gondii tachyzoites. The dissemination of T. gondii was monitored by in vivo bioluminescence imaging in real time for 7 days and by plaque formation. The inflammatory response was analysed in bronchoalveolar lavage (BAL) fluid, and by assessment of morphological changes and immune responses in lung and spleen.
  
  
  RESULTS
  There were no differences in parasite distribution between mice only inoculated with T. gondii or those mice pre-exposed for 2 days to SWCNT before parasite inoculum. Lung and spleen histology and inflammation markers in BAL fluid reflected the effects of SWCNT exposure and T. gondii injection, respectively. We also noted that CD11c positive dendritic cells but not F4/80 positive macrophages retained SWCNT in the lungs 9 days after pharyngeal aspiration. However, co-localization of T. gondii with CD11c or F4/80 positive cells could not be observed in lungs or spleen. Pre-exposure to SWCNT did not affect the splenocyte response to T. gondii.
  
  
  CONCLUSIONS
  Taken together, our data indicate that pre-exposure to SWCNT does not enhance or suppress the early immune response to T. gondii in mice.
authors.affiliation: Institute of Environmental Medicine, Division of Molecular Toxicology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Linda
authors.initials: L
authors.lastname: Swedin
authors.forename: Romanico
authors.initials: R
authors.lastname: Arrighi
authors.forename: Britta
authors.initials: B
authors.lastname: Andersson-Willman
authors.forename: Ashley
authors.initials: A
authors.lastname: Murray
authors.forename: Yunying
authors.initials: Y
authors.lastname: Chen
authors.forename: Mikael C I
authors.initials: MC
authors.lastname: Karlsson
authors.forename: Susanna Kumlien
authors.initials: SK
authors.lastname: Georén
authors.forename: Alexey V
authors.initials: AV
authors.lastname: Tkach
authors.forename: Anna A
authors.initials: AA
authors.lastname: Shvedova
authors.forename: Bengt
authors.initials: B
authors.lastname: Fadeel
authors.forename: Antonio
authors.initials: A
authors.lastname: Barragan
authors.forename: Annika
authors.initials: A
authors.lastname: Scheynius
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D007111:Immunity, Cellular / Q000187:drug effects* / Q000276:immunology; D007442:Intubation, Intratracheal; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D037742:Nanotubes, Carbon / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced* / Q000276:immunology / Q000382:microbiology; D011658:Pulmonary Fibrosis; D013154:Spleen / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D014122:Toxoplasma / Q000472:pathogenicity*; D014124:Toxoplasmosis, Animal / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology
chemical_list: D037742:Nanotubes, Carbon