J. Exp. Med., Volume 188, Number 9, November 2, 1998 1587-1592

Immunoglobulin E-dependent Active Fatal Anaphylaxis in Mast Cell-deficient Mice

By Il Hwan Choi,^* Young Min Shin,^* Jae Seung Park,^* Moo Sam Lee, Eue Hyeog Han, Ok Hee Chai, Shun Young Im,^§ Tai  You Ha,^* and Hern-Ku Lee^*

From the ^* Department of Immunology and Institute for Medical Science, and the  Department of Anatomy, Chonbuk National University Medical School, Chonju, Chonbuk, 561-182, Republic of Korea; and the ^§ Department of Microbiology and Hormone Research Center, College of Natural Science, Chonnam National University, Kwangju, Chonnam, 500-757, Republic of Korea

Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell-deficient WBB6F1- W/W^v (W/W^v) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/W^v mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/W^v mice. Administration of monoclonal anti-IL-4 antibody completely prevented the fatal reactions, and the effect of anti-IL-4 was associated with its suppressive activity on Pen V-specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/W^v mice, high levels of PAF in the circulation after challenge in both +/+ and W/W^v mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.

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