title: Diesel exhaust exposure favors TH2 cell recruitment in nonatopic subjects by differentially regulating chemokine production.
abstract: BACKGROUND
  The prevalence of allergic diseases has increased in the last 20 years, and a number of studies have shown that diesel exhaust particle-associated polyaromatic hydrocarbons can exacerbate the allergic reaction. Much less is known about their potential capacity to generate a T(H)2-type allergic reaction in nonatopic subjects.
  
  
  OBJECTIVE
  The aim of this study was to test the hypothesis that diesel exhaust exposure might favor, in nonatopic donors, T(H)2-type cell recruitment, either through increased production of T(H)2-attracting chemokines or decreased production of T(H)1-attracting chemokines.
  
  
  METHODS
  PBMCs from nonatopic donors were incubated with diesel exhaust particle-polyaromatic hydrocarbons, and the supernatants were evaluated for the presence of pro-T(H)1 chemokines (IFN-gamma-induced protein 10 and monokine Induced by IFN-gamma) and pro-T(H)2 chemokines (macrophage-derived chemokine, I-309, and pulmonary and activation-regulated chemokine) by means of ELISA. The functional effect was evaluated by using chemotaxis assays with polarized T(H)1 and T(H)2 cells.
  
  
  RESULTS
  Diesel exhaust exposure of PBMCs from nonatopic donors induced a late increase after 48 hours in pulmonary and activation-regulated chemokine mediated by IL-13 and a decrease in IFN-gamma-induced protein 10 levels selectively at both the protein and mRNA levels. The functional effect of these chemokine variations resulted in an enhanced chemotaxis of T(H)2, but not T(H)1, cells.
  
  
  CONCLUSIONS
  These findings show that diesel exhaust exposure might be involved in the genesis of allergic diseases by differentially regulating chemokines favoring the recruitment of T(H)2 cells in nonatopic subjects.
  
  
  CONCLUSIONS
  Environmental factors, especially air pollution, might favor the genesis of allergic diseases.
authors.affiliation: INSERM U-774, Institut Pasteur de Lille, 59 019 Lille Cedex, France.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chang
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Sénéchal
authors.forename: Patricia
authors.initials: P
authors.lastname: de Nadai
authors.forename: Cécile
authors.initials: C
authors.lastname: Chenivesse
authors.forename: Jules
authors.initials: J
authors.lastname: Gilet
authors.forename: Han
authors.initials: H
authors.lastname: Vorng
authors.forename: Benjamin
authors.initials: B
authors.lastname: Legendre
authors.forename: André-Bernard
authors.initials: AB
authors.lastname: Tonnel
authors.forename: Benoît
authors.initials: B
authors.lastname: Wallaert
authors.forename: Philippe
authors.initials: P
authors.lastname: Lassalle
authors.forename: Anne
authors.initials: A
authors.lastname: Tsicopoulos
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D018925:Chemokines / Q000096:biosynthesis; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology* / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity*; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D018925:Chemokines; D011084:Polycyclic Aromatic Hydrocarbons; D001335:Vehicle Emissions