Wheat allergy is a major type of food allergy with the potential for life-threatening anaphylactic reactions. Common wheat, Triticum aestivum (hexaploid, AABBDD genome), was developed using tetraploid wheat (AABB genome) and the ancient diploid wheat progenitor (DD genome)-Aegilops tauschii. The potential allergenicity of gluten from ancient diploid wheat is unknown. In this study, using a novel adjuvant-free gluten allergy mouse model, we tested the hypothesis that the glutenin extract from this ancient wheat progenitor will be intrinsically allergenic in this model. The ancient wheat was grown, and wheat berries were used to extract the glutenin for testing. A plant protein-free colony of Balb/c mice was established and used in this study. The intrinsic allergic sensitization potential of the glutenin was determined by measuring IgE response upon transdermal exposure without the use of an adjuvant. Clinical sensitization for eliciting systemic anaphylaxis (SA) was determined by quantifying the hypothermic shock response (HSR) and the mucosal mast cell response (MMCR) upon intraperitoneal injection. Glutenin extract elicited a robust and specific IgE response. Life-threatening SA associated and a significant MMCR were induced by the glutenin challenge. Furthermore, proteomic analysis of the spleen tissue revealed evidence of in vivo Th2 pathway activation. In addition, using a recently published fold-change analysis method, several immune markers positively and negatively associated with SA were identified. These results demonstrate for the first time that the glutenin from the ancient wheat progenitor is intrinsically allergenic, as it has the capacity to elicit clinical sensitization for anaphylaxis via activation of the Th2 pathway in vivo in mice.

Anaphylaxis is a life-threatening response to various types of allergens. Early recognition and management are crucial for reducing mortality. This case report highlights a 31-year-old male with a background of hypertension who presented to the emergency department with nausea, vomiting, right flank pain, headache, and elevated blood pressure (BP) of 212/134 mmHg. The patient was started on stat captopril 12.5 mg tablet and stat amlodipine 5 mg tablet for his high BP and stat diclofenac 75 mg (1 mg/kg) intramuscular (IM) for his flank pain. Two minutes later the patient started developing swelling of his mucosal membranes with no urticaria or rashes and his BP suddenly dropped and was unrecordable. First-line management was immediately initiated including the administration of two standard adult doses of IM epinephrine of 500 mcg each with a 5-minute interval. The BP remained undetectable; accordingly, a third IM epinephrine dose of 500 mcg was administered along with an intravenous (IV) epinephrine drip initiated at a rate of 4 mcg/min. The BP became 60/40 mmHg but kept dropping, thus an IV epinephrine bolus of 300 mcg (4 mcg/kg) was given along with the ongoing IV epinephrine drip. BP increased to 126/75 mmHg. While on the IV epinephrine drip the BP dropped again to 88/59 mmHg, a second IV epinephrine bolus of 200 mcg (2.6 mcg/kg) was given and the BP became 140/90 mmHg and recovery was achieved. Emergency cases require immediate recognition and intervention. Currently, IM epinephrine is the primary treatment for anaphylaxis. We hope our case report contributes to the database on severe refractory anaphylaxis by discussing a successful case where IV bolus epinephrine was used to prevent imminent cardiovascular collapse. Highlighting the need for appropriate escalation of management given the availability of physicians with expertise.