title: Effects of nano particles on antigen-related airway inflammation in mice.
abstract: BACKGROUND
  Particulate matter (PM) can exacerbate allergic airway diseases. Although health effects of PM with a diameter of less than 100 nm have been focused, few studies have elucidated the correlation between the sizes of particles and aggravation of allergic diseases. We investigated the effects of nano particles with a diameter of 14 nm or 56 nm on antigen-related airway inflammation.
  
  
  METHODS
  ICR mice were divided into six experimental groups. Vehicle, two sizes of carbon nano particles, ovalbumin (OVA), and OVA + nano particles were administered intratracheally. Cellular profile of bronchoalveolar lavage (BAL) fluid, lung histology, expression of cytokines, chemokines, and 8-hydroxy-2'-deoxyguanosine (8-OHdG), and immunoglobulin production were studied.
  
  
  RESULTS
  Nano particles with a diameter of 14 nm or 56 nm aggravated antigen-related airway inflammation characterized by infiltration of eosinophils, neutrophils, and mononuclear cells, and by an increase in the number of goblet cells in the bronchial epithelium. Nano particles with antigen increased protein levels of interleukin (IL)-5, IL-6, and IL-13, eotaxin, macrophage chemoattractant protein (MCP)-1, and regulated on activation and normal T cells expressed and secreted (RANTES) in the lung as compared with antigen alone. The formation of 8-OHdG, a proper marker of oxidative stress, was moderately induced by nano particles or antigen alone, and was markedly enhanced by antigen plus nano particles as compared with nano particles or antigen alone. The aggravation was more prominent with 14 nm of nano particles than with 56 nm of particles in overall trend. Particles with a diameter of 14 nm exhibited adjuvant activity for total IgE and antigen-specific IgG1 and IgE.
  
  
  CONCLUSIONS
  Nano particles can aggravate antigen-related airway inflammation and immunoglobulin production, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, by the increased local expression of IL-5 and eotaxin, and also by the modulated expression of IL-13, RANTES, MCP-1, and IL-6.
authors.affiliation: Inhalation Toxicology and Pathophysiology Research Team, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan. inoue.kenichirou@nies.go.jp
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Miho
authors.initials: M
authors.lastname: Sakurai
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Kaori
authors.initials: K
authors.lastname: Sadakane
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects; D000818:Animals; D000941:Antigens / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000276:immunology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D049329:Nanostructures / Q000633:toxicity*; D010047:Ovalbumin; D010316:Particle Size; D011014:Pneumonia / Q000209:etiology* / Q000276:immunology* / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000209:etiology* / Q000276:immunology* / Q000473:pathology
chemical_list: D000393:Air Pollutants; D000941:Antigens; D016207:Cytokines; D010047:Ovalbumin