Food, drug, insect sting allergy, and anaphylaxisInduction and suppression of allergic diarrhea and systemic anaphylaxis in a murine model of food allergy
Section snippets
Mice
BALB/c-background wild-type (WT) and transgenic mice in which an IL-9 transgene is regulated by the intestinal fatty acid–binding protein promoter (iIL-9 Tgn mice),15 BALB/c-background polymeric immunoglobulin receptor (pIgR)–deficient mice (Jackson Laboratories, Bar Harbor, Me),16 BALB/c-background J-chain–deficient mice (a gift from Dennis Metzger, Albany Medical College, Albany, NY),17 and BALB/c-background FcγRIIb–deficient mice18 were all bred in house. All experimental procedures were
Passive immunization with IgE antibody is sufficient for antigen ingestion to induce shock, but not diarrhea, in immunologically naive mice
Initial experiments determined whether increased levels of antigen-specific IgE antibody are sufficient for ingestion of the targeted antigen to induce systemic shock, allergic diarrhea, or both. By itself, intravenous injection of WT mice with IgE anti-TNP mAb did not induce shock (hypothermia) or diarrhea (data not shown); however, OG of these IgE-primed mice the next day with 50 mg of TNP-BSA induced shock (hypothermia), although it did not induce diarrhea (Fig 1, A). To determine whether
Discussion
The studies described here (1) explain how allergic diarrhea and systemic anaphylaxis can each occur by itself in patients with food allergy and (2) demonstrate that even allergic diarrhea requires systemic absorption of ingested allergen. Our observation that passive immunization with IgE anti-TNP, followed by ingestion of TNP-BSA, causes shock but not diarrhea indicates that basal mast cell numbers and quantities of antigen absorption are sufficient to induce shock but not diarrhea. This
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2020, Advances in ImmunologyCitation Excerpt :However there is more direct evidence, including the studies of Daeron and colleagues, for the alternative hypothesis that IgG binding to the inhibitory Fc receptor FcγRIIb delivers suppressive signals to mouse and human mast cells and basophils, dampening FcɛRI-driven activation via direct effector cell interaction and intracellular signaling pathways (Cassard, Jonsson, Arnaud, & Daeron, 2012; Daeron, Malbec, Latour, Arock, & Fridman, 1995). Both mechanisms of action have been shown to block systemic anaphylaxis in mice, although inhibition of diarrhea in an experimental food allergy model by monoclonal IgG1 appears to be FcγRIIb-indendent (Kucuk et al., 2012; Strait, Morris, & Finkelman, 2006). Our own studies of the inhibitory mechanisms of IgG that is induced following OIT using serum from human patients and mice are most consistent with a receptor mediated inhibitory mechanism of IgG (Burton et al., 2014).
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Human IgE-independent systemic anaphylaxis
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Supported by a Department of Veterans Affairs Merit Award (to F.D.F.), National Institutes of Health (NIH) grant R01 AI073553 (to S.H.), and an NIH T32 Training Grant (to Z.Y.K.).
Disclosure of potential conflict of interest: S. Hogan has consultant arrangements with Immune Pharmaceuticals and receives research support from the National Institutes of Health. The rest of the authors declare that they have no relevant conflicts of interest.