Abstract
Food allergies are a steadily increasing health and economic problem. Immunologically, food allergic reactions are caused by pathological, allergen-specific Th2 responses resulting in IgE-mediated mast cell degranulation and associated inflammatory reactions. Clinically, food allergies are characterized by local inflammation of the mouth mucosa, the face, the throat, the gastrointestinal tract, are frequently paralleled by skin reactions, and can result in life-threatening anaphylactic reactions. To better understand food allergies and establish novel treatment options, mouse models are indispensable. This review discusses the available mouse food allergy models, dividing them into four categories: (1) adjuvant-free mouse models, (2) mouse models relying on adjuvants to establish allergen-specific Th2 responses, (3) mouse models using genetically-modified mouse strains to allow for easier sensitization, and (4) humanized mouse models in which different immunodeficient mouse strains are reconstituted with human immune or stem cells to investigate humanized immune responses. While most of the available mouse models can reproducibly portray the immunological parameters of food allergy (Th2 immune responses, IgE production and mast cell activation/expansion), so far, the recreation of the clinical parameters has proven more difficult. Therefore, up to now none of the available mouse models can reproduce the complete human pathology.
Highlights
Upon second contact with mast cell and eosinophil activation and local release of histamine, cytokines, proteases, hormones, the allergen the allergic reaction is triggered by the cross-linking of the surface bound IgE antibodies and other pro-inflammatory mediators in a process called degranulation which causes the allergic resulting in the degranulation of the mast cell associated with the release of large amounts of proinflammation and the associated symptoms (Figure 1)
Studies have shown that rodents can be sensitized to food allergens either with or without the use of additional adjuvants, resulting in allergic responses upon re-exposure to the respective allergens that reflect allergic responses observed in human patients [33]
Not as commonly used as mice, other animal models not covered in this review like guinea pig, rat, or neonatal swine might prove useful for certain well as mast cell activation and expansion (Figure 6)
Summary
With a prevalence of 8% in children and 4% in adults, food allergies are a growing health and economic problem [1,2,3]. The frequency of food allergies is increasing, and their severity. 40% of food allergic children were reported to suffer from severe type reactions (e.g., shortness of breath, shock type reactions) upon contact with the respective allergen [2]. When analyzing data from the USA, food allergies cause 50,000 visits to the emergency room per year [4] with 150 to 200 fatal reactions [2] and are responsible for approximately 500 million USD in both direct (e.g., hospital care and doctor visits) and indirect (e.g., loss of work force) costs [5]. In terms of allergen sources, 90% of food allergic reactions are caused by either egg, milk, wheat, soy, peanuts, tree nuts, shellfish, or fish (the so-called “red flag foods“) [6,7]
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