Systemic anaphylaxis in the mouse can be mediated largely through IgG, and Fc gamma RIII - Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG(1)-dependent passive anaphylaxis

We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE- or IgG(1)-dependent anaphylaxis, in mice lacking either the Fc(epsilon)RI alpha chain or the FcR gamma chain common to Fc(epsilon)RI and Fc gamma RI/III, or in mice lacking mast cells (Kit(W)/Kit(W-v) mice), and compared the responses to those in the corresponding wild-type mice. We found that the FcR gamma chain is required for the death, as well as for most of the pathophysiological changes, associated with active anaphylaxis or IgE- or IgG(1)-dependent passive anaphylaxis. Moreover, some of the physiological changes associated with either active, or IgG(1)-dependent passive, anaphylactic responses were significantly greater in Fc(epsilon)RI alpha chain -/- mice than in the corresponding normal mice. Finally, while both Kit(W)/Kit(W-v) and congenic +/+ mice exhibited fatal active anaphylaxis, mast cell-deficient mice exhibited weaker physiological responses than the corresponding wild-type mice in both active and IgG(1)-dependent passive systemic anaphylaxis. Our findings strongly suggest that while IgE antibodies and Fc(epsilon)RI may influence the intensity and/or kinetics of some of the pathophysiological changes associated with active anaphylaxis in the mouse, the mortality associated with this response can be mediated largely by IgG(1) antibodies and Fc gamma-RIII.