title: Prior oral exposure to environmental immunosuppressive chemicals methoxychlor, parathion, or piperonyl butoxide aggravates allergic airway inflammation in NC/Nga mice.
abstract: BACKGROUND
  Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of respiratory tract allergies, such as allergic rhinitis and asthma.
  
  
  OBJECTIVE
  We investigated the association between environmental immunosuppressive chemicals and the allergic airway inflammation development.
  
  
  METHODS
  We used a mouse model of ovalbumin (OVA)-induced allergic airway inflammation. NC/Nga mice were exposed orally to pesticides parathion (an organophosphate compound) or methoxychlor (an organochlorine compound), or to an insecticide synergist piperonyl butoxide, prior to OVA intraperitoneal sensitization and inhalation challenge. We assessed serum IgE levels, B-cell counts, cytokine production, IgE production in hilar lymph nodes, eosinophil counts, chemokine levels in bronchoalveolar lavage fluid, and cytokine gene expression in the lung.
  
  
  RESULTS
  Exposure to environmental immunosuppressive chemicals markedly increased serum IgE - IgE-positive B-cells, IgE and cytokines in lymph nodes - eosinophils and chemokines in BALF - IL-10a and IL-17 in the lung.
  
  
  CONCLUSIONS
  Allergic airway inflammation can be aggravated by prior exposure to immunosuppressive environmental chemicals.
authors.affiliation: Laboratory of Immunotoxicology and Acute Toxicology, Toxicology Division, Institute of Environmental Toxicology, Uchimoriya-machi 4321, Joso-shi, Ibaraki 303-0043, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Nishino
authors.forename: T
authors.initials: T
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Tajima
authors.forename: L
authors.initials: L
authors.lastname: Miyashita
authors.forename: Y
authors.initials: Y
authors.lastname: Watanabe
authors.forename: H
authors.initials: H
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Kosaka
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001991:Bronchitis / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006967:Hypersensitivity / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D007166:Immunosuppressive Agents / Q000633:toxicity*; D018836:Inflammation Mediators / Q000633:toxicity*; D008731:Methoxychlor / Q000008:administration & dosage / Q000633:toxicity*; D051379:Mice; D010278:Parathion / Q000008:administration & dosage / Q000633:toxicity*; D010882:Piperonyl Butoxide / Q000633:toxicity*; D011897:Random Allocation; D013997:Time Factors
chemical_list: D007166:Immunosuppressive Agents; D018836:Inflammation Mediators; D010278:Parathion; D010882:Piperonyl Butoxide; D008731:Methoxychlor