title: Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice.
abstract: BACKGROUND
  Eosinophils are selectively recruited into the tissues during chronic allergic inflammation. IgE is considered an initiator of the allergic reaction; however, the roles of IgE in allergic inflammation are not fully understood.
  
  
  OBJECTIVE
  We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation.
  
  
  METHODS
  BALB/c mice were actively sensitized with ragweed extract and passively sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP-ovalbumin (OVA). Immediate anaphylactic responses were examined by monitoring vascular permeability and by measuring histamine content in peritoneal lavage fluids. Late-phase allergic responses were examined by total cell counts and cell differentials.
  
  
  RESULTS
  Mice sensitized and challenged with ragweed showed immediate anaphylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities after 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphylactic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic responses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-challenged animals recruited both eosinophils and neutrophils, but DNP-OVA-challenged animals recruited only neutrophils. Finally, after active sensitization and challenge with ragweed, mast cell-deficient mice (WBB6F1-W/W(v)) lacked the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1-+/+).
  
  
  CONCLUSIONS
  Interaction of antigen with IgE antibody is insufficient to provoke eosinophilic inflammation in mice.
authors.affiliation: Department of Internal Medicine, Mayo Medical and Graduate Schools, Mayo Clinic, Rochester, MN 55905, USA.
authors.forename: M
authors.initials: M
authors.lastname: Kaneko
authors.forename: A
authors.initials: A
authors.lastname: Schimming
authors.forename: G J
authors.initials: GJ
authors.lastname: Gleich
authors.forename: H
authors.initials: H
authors.lastname: Kita
mesh_terms: D019297:2,4-Dinitrophenol / Q000276:immunology; D000707:Anaphylaxis / Q000209:etiology* / Q000473:pathology; D000818:Animals; D000941:Antigens; D004195:Disease Models, Animal; D004804:Eosinophils; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007114:Immunization; D007116:Immunization, Passive; D007249:Inflammation / Q000209:etiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000473:pathology*; D010538:Peritonitis / Q000276:immunology; D011058:Pollen; D017455:Receptors, IgE / Q000502:physiology*
chemical_list: D000941:Antigens; D017455:Receptors, IgE; D019297:2,4-Dinitrophenol