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This article is part of the supplement: Canadian Society of Allergy and Clinical Immunology Annual Scientific Meeting 2011

Open Access Open Badges Meeting abstract

Testing an emerging animal model for use in the allergenicity assessment of food

David E Lefebvre1*, Nikia Ross1, Laurie Coady1, Cheryl Armstrong1, Susan Gurofsky1, Ivan Curran1, Tim Schrader1, Don Caldwell2 and Genevieve S Bondy1

  • * Corresponding author: David E Lefebvre

Author Affiliations

1 Toxicology Research Division, Bureau of Chemical Safety, Food Directorate, Health Canada, Ottawa, ON, K1A 0L2, Canada

2 Scientific Services Division, Bureau of Chemical Safety, Food Directorate, Health Canada, Ottawa, ON, K1A 0L2, Canada

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Allergy, Asthma & Clinical Immunology 2011, 7(Suppl 2):A1  doi:10.1186/1710-1492-7-S2-A1

The electronic version of this article is the complete one and can be found online at:

Published:14 November 2011

© 2011 Lefebvre et al; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The regulatory assessment of novel food includes tests for allergy. The World Health Organization suggests tests in an animal model of allergy despite the lack of a validated model. We aimed to confirm if C3H/HeJ mice would respond to food of high allergenic potential (peanut), but not to food of low allergenic potential (turkey, potato, spinach).


In the first study, C3H/HeJ mice were orally treated, once per week for two weeks, with adjuvant and 0 or 2 mg of peanut or turkey. A second study used adjuvant and 0, 0.1, 1 or 2 mg of peanut, potato or spinach. Blood IgE antibodies and spleen interleukin-4 were quantified.


Mice treated with 2 mg peanut developed peanut-specific IgE levels which were significantly higher than control mice (p<0.001, n=10/group). Mice treated with 2 mg turkey developed a similar IgE response to turkey (p<0.001, n=10/group). In the second study, allergy was only triggered in one of ten mice treated with 2 mg peanut. Two of ten mice exposed to 1 mg potato had a response. There were no IgE responders to spinach. Spleen cells from both the peanut- and the spinach-treated mice secreted more allergy-promoting interleukin-4 than controls (p<0.01, n=7-24/group). Levels were not modified in potato-treated mice.


C3H/HeJ mice developed food allergy markers to peanut. However, the incidence varied between experiments. Some mice developed a similar response to foods with low allergenic potential. Thus, this model may not be appropriate for safety assessment of novel food.