title: Prior or coinstantaneous oral exposure to environmental immunosuppressive agents aggravates mite allergen-induced atopic dermatitis-like immunoreaction in NC/Nga mice.
abstract: BACKGROUND
  Immunosuppressive environmental chemicals may increase the potency of allergens and thereby play a role in the development of allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (AD).
  
  
  OBJECTIVE
  This study's primary objective was to examine the mechanisms behind the development of allergic diseases and immunosuppression induced by some environmental chemicals. We focused on the aggravation of AD by the organophosphorus pesticide O,O-diethyl-O-4-nitro-phenylthiophosphate (parathion) and the organochlorine pesticide 1,1,1-trichloro-2,2-bis(4-methoxyphenyl)ethane (methoxychlor), in NC/Nga mice sensitized with extract of Dermatophagoides farinae (Df).
  
  
  METHODS
  NC/Nga mice were exposed orally to parathion or methoxychlor prior or coinstantaneous with sensitization with Df. The mice were subsequently challenged with Df. One day after the last challenge with Df, we analyzed dermatitis severity and expression of genes in the ear auricle, immunoglobulin (Ig) E and IgG(2a) levels in serum, and in auricular lymph nodes, T- or B-cell numbers and cytokine production.
  
  
  RESULTS
  Prior exposure to parathion or methoxychlor induced marked increases in the following: dermatitis severity and gene expression in the ear auricle, IgE and IgG(2a) levels in serum, expression of surface antigens on helper T-cell and IgE-positive B-cell, production of Th1 and Th2 cytokines, and production of IgE in auricular lymph-node cells. In contrast, coinstantaneous exposure to parathion or methoxychlor yielded, at most, small but significant decreases in all parameters.
  
  
  CONCLUSIONS
  Our results indicate that atopic dermatitis can be aggravated by prior exposure to immunosuppressive environmental chemicals.
authors.affiliation: Institute of Environmental Toxicology, Ibaraki 303-0043, Japan. fukuyama@iet.or.jp
authors.forename: T
authors.initials: T
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Tajima
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
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; D039741:Antigens, Dermatophagoides / Q000008:administration & dosage* / Q000276:immunology / Q000633:toxicity; D003876:Dermatitis, Atopic / Q000139:chemically induced* / Q000276:immunology* / Q000469:parasitology; D040001:Dermatophagoides farinae / Q000187:drug effects / Q000276:immunology*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000633:toxicity*; D007306:Insecticides / Q000633:toxicity; D008731:Methoxychlor / Q000633:toxicity*; D051379:Mice; D010278:Parathion / Q000633:toxicity*
chemical_list: D039741:Antigens, Dermatophagoides; D007166:Immunosuppressive Agents; D007306:Insecticides; D010278:Parathion; D008731:Methoxychlor