Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice.
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.
Kaneko
M
M
Department of Internal Medicine, Mayo Medical and Graduate Schools, Mayo Clinic, Rochester, MN 55905, USA.
Schimming
A
A
Gleich
G J
GJ
Kita
H
H
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*
D000941:Antigens; D017455:Receptors, IgE; D019297:2,4-Dinitrophenol