title: Cutaneous or respiratory exposures to peanut allergens in mice and their impacts on subsequent oral exposure.
abstract: BACKGROUND
  Recent data suggested that non-gastrointestinal exposure can lead to sensitisation to food allergens. We thus assessed the immune impact of respiratory or cutaneous exposure to peanut proteins on non-altered epithelium and investigated the effect of such pre-exposure on subsequent oral administration of peanut.
  
  
  METHODS
  BALB/cJ mice were exposed to purified Ara h 1 or to a non-defatted roasted peanut extract (PE) by simple deposit of allergens solutions on non-altered skin or in the nostrils. Exposures were performed 6 times at weekly intervals. Pre-exposed mice then received intra-gastric administrations of PE alone or in the presence of the Th2 mucosal adjuvant cholera toxin (CT). The specific humoral and cellular immune response was assessed throughout the protocol.
  
  
  RESULTS
  Both cutaneous and respiratory exposures led to the production of specific IgG1. Local and systemic IL-5 and IL-13 production were also evidenced, demonstrating activation of specific Th2 cells. This effect was dose-dependent and most efficient via the respiratory route. Moreover, these pre-exposures led to the production of specific IgE antibodies after gavage with PE, whatever the presence of CT.
  
  
  CONCLUSIONS
  Cutaneous or respiratory exposures to peanut induce Th2 priming in mice. Moreover, pre-exposures promote further sensitisation via the oral route without the use of CT; this proposes a new adjuvant-free experimental model of sensitisation to food that may reflect a realistic exposure pattern in infants. These results also suggest that non-gastrointestinal peanut exposure should be minimised in high-risk infants, even those with non-altered skin, to potentially reduce allergic sensitisation to this major food allergen.
authors.affiliation: INRA, UR496 Immuno-Allergie Alimentaire, CEA/IBiTeC-S/SPI, CEA de Saclay, Gif-sur-Yvette, France.
authors.forename: Sophie
authors.initials: S
authors.lastname: Wavrin
authors.forename: Hervé
authors.initials: H
authors.lastname: Bernard
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Wal
authors.forename: Karine
authors.initials: K
authors.lastname: Adel-Patient
mesh_terms: D000276:Adjuvants, Immunologic / Q000008:administration & dosage; D000279:Administration, Cutaneous; D000280:Administration, Inhalation; D000284:Administration, Oral; D000485:Allergens / Q000008:administration & dosage / Q000276:immunology*; D000818:Animals; D052179:Antigens, Plant / Q000008:administration & dosage / Q000276:immunology*; D010367:Arachis / Q000276:immunology*; D002772:Cholera Toxin / Q000008:administration & dosage / Q000276:immunology; D004195:Disease Models, Animal; D004781:Environmental Exposure; D005260:Female; D006023:Glycoproteins / Q000008:administration & dosage / Q000276:immunology*; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000276:immunology; D018793:Interleukin-13 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology; D008565:Membrane Proteins; D051379:Mice; D008807:Mice, Inbred BALB C; D021183:Peanut Hypersensitivity / Q000276:immunology*; D010936:Plant Extracts / Q000008:administration & dosage / Q000276:immunology; D010940:Plant Proteins / Q000008:administration & dosage / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000276:Adjuvants, Immunologic; D000485:Allergens; D052179:Antigens, Plant; C500889:Ara h 1 protein, Arachis hypogaea; D006023:Glycoproteins; D007074:Immunoglobulin G; D018793:Interleukin-13; D015848:Interleukin-5; D008565:Membrane Proteins; D010936:Plant Extracts; D010940:Plant Proteins; D002772:Cholera Toxin