title: Components of diesel exhaust particles differentially affect Th1/Th2 response in a murine model of allergic airway inflammation.
abstract: BACKGROUND
  Diesel exhaust particles (DEP) can enhance various respiratory diseases. However, it is unclear as to which components in DEP are associated with the enhancement. We investigated the effects of DEP components on antigen-related airway inflammation, using residual carbonaceous nuclei of DEP after extraction (washed DEP), extracted organic chemicals (OC) in DEP (DEP-OC), and DEP-OC plus washed DEP (whole DEP) in the presence or absence of ovalbumin (OVA).
  
  
  METHODS
  Male ICR mice were intratracheally administrated with OVA and/or DEP components. We examined the cellular profile of bronchoalveolar lavage (BAL) fluid, histological changes, lung expression of inflammatory molecules, and antigen-specific production of IgG1 in the serum.
  
  
  RESULTS
  DEP-OC, rather than washed DEP, enhanced infiltration of inflammatory cells into BAL fluid, magnitude of airway inflammation, and proliferation of goblet cells in the airway epithelium in the presence of OVA, which was paralleled by the enhanced lung expression of eotaxin and IL-5 as well as the elevated concentration of OVA-specific IgG1. In contrast, washed DEP with OVA showed less change and increased the lung expression of IFN-gamma. The combination of whole DEP and OVA caused the most remarkable changes in the entire enhancement, which was also accompanied by the enhanced expression of IL-13 and macrophage inflammatory protein-1 alpha.
  
  
  CONCLUSIONS
  DEP-OC, rather than washed DEP, exaggerated allergic airway inflammation through the enhancement of T-helper type 2 responses. The coexistence of OC with carbonaceous nuclei caused the most remarkable aggravation. DEP components might diversely affect various types of respiratory diseases, while whole DEP might mostly aggravate respiratory diseases.
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: K-I
authors.initials: KI
authors.lastname: Inoue
authors.forename: T
authors.initials: T
authors.lastname: Ichinose
authors.forename: K
authors.initials: K
authors.lastname: Sadakane
authors.forename: S
authors.initials: S
authors.lastname: Yoshino
authors.forename: K
authors.initials: K
authors.lastname: Yamaki
authors.forename: T
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: K
authors.initials: K
authors.lastname: Hayakawa
mesh_terms: D000276:Adjuvants, Immunologic; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D018925:Chemokines / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood; D015848:Interleukin-5 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010047:Ovalbumin / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000276:Adjuvants, Immunologic; D018925:Chemokines; D016207:Cytokines; D007074:Immunoglobulin G; D015848:Interleukin-5; D001335:Vehicle Emissions; D010047:Ovalbumin