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 c hronic allergic inflammation. IgE is considered an initiator of the allergi c reaction; however, the roles of IgE in allergic inflammation are not full y understood. Objective: We tested the hypothesis that antigen interaction with specific IgE antibody provokes eosinophilic inflammation. Methods: BALB/c mice mere actively sensitized dth ragweed extract and passi vely sensitized with anti-dinitrophenyl (anti-DNP) mouse IgE and challenged intraperitoneally by injecting either ragweed extract or DNP-ovalbumin (OV A). Immediate anaphylactic responses mere examined by monitoring vascular p ermeability 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 anaph ylactic responses followed by temporal increases in neutrophils at 3 to 12 hours and sustained increases in eosinophils in their peritoneal cavities a fter 24 hours. Double-sensitized mice (ie, sensitized actively for ragweed and passively for DNP-OVA) challenged with ragweed showed immediate anaphyl actic responses and peritoneal eosinophilia at 48 hours. Double-sensitized mice challenged with DNP-OVA showed comparable immediate anaphylactic respo nses but no peritoneal eosinophilia. Furthermore, at 8 hours, ragweed-chall enged animals recruited both eosinophils and neutrophils, but DNP-OVA-chall enged animals recruited only neutrophils. Finally, after active sensitizati on and challenge with ragweed, mast cell-deficient mice (WBB6F1-W/W-v) lack ed the immediate response but showed comparable eosinophil accumulation as their litter mate controls (WBB6F1-+/+). Conclusion: Interaction of antigen dth IgE antibody is insufficient to prov oke eosinophilic inflammation in mice.