The PATHOGENesis of food allergy
- 1Division of Clinical Immunology and Allergy, Children's Hospital of Los Angeles, United States
- 2University of Southern California, United States
Food allergy has a negative impact on the quality of life and nutrition. In addition, it can lead to life-threatening reactions. The pathogenesis of food allergy is still not fully understood. Many young children develop food allergy with no known prior ingestion of the food allergen in question. The strong connection between food allergy and atopic dermatitis has been well-documented. While the prevalence of food allergy in the general pediatric population is 4 to 5%, the prevalence of food allergy in atopic dermatitis is at least 20% (1). This connection between food allergy and atopic dermatitis has led to the suggestion that the skin may be the site of food IgE sensitization, leading to food allergy. The dual-allergen-exposure hypothesis suggests that food allergens are sensitized via eczema, whereas early gastro-intestinal exposure leads to tolerance (2). This hypothesis is supported by multiple basic studies that provide evidence for IgE sensitization via the skin (reviewed in Ref. 3). In addition, it has been shown that environmental level of peanut allergens is increased in children who developed peanut allergy (4). The early introduction of peanut has led to the prevention of peanut allergy (4). On the other hand, early introduction of egg has not been as successful (6). It is believed that egg allergy develops much earlier before infants are capable of crawling or eating solid food. During this age, environmental and gastro-intestinal contact with egg allergens are unlikely. An alternative explanation is proposed here that some microbial proteins share common sequences with egg allergens, and that these microbial proteins could be a source of IgE sensitization which leads to the development of egg allergy.
The current hypothesis predicts the presence of microbial proteins that are homologous to egg allergens (see Table 1). Prospective studies may be carried out to look for these microbial pathogens in atopy-prone neonates and correlate with neonates who eventually develop egg allergy. These microbial pathogens can also be inoculated in animal models to show the development of specific IgE that cross-react with egg allergens. Atopy-prone neonates who are born to parent with atopic dermatitis, asthma or allergic rhinitis have inherent skin barrier defects that predispose them to develop atopic dermatitis. Microbial pathogens are capable of evading these barrier defects to interact with the cutaneous immune system in these children . The processing of microbial proteins by antigen-presenting cells and subsequent presentation of antigenic peptides to T helper type 2 cells leads to the production of IL-4 and IL-13, which induce B cells to express specific IgE molecules. Bacterial allergy has been described more than half a century ago (7). It is also known that specific IgE to staphylococcal toxins can develop in young children with atopic dermatitis (8). Bacteria such as bacteroides can be acquired during birth or they can be part of neonates’ microbiome (9). The skin also contains a wide array of microbial pathogens that can participate in the development of allergy (10). More recent data suggests that many microbial organisms (eg. proteobacteria and archaea) previously thought to exist only in the environment such as soil, fresh or marine waters are now found to be part of the human skin microbiome (11, 12). The current proposal is conceptual that microbial proteins can be a sensitizing source in the development of food allergy. Whether these microbial pathogens have a direct interaction with neonates, leading to the development of specific IgE, remains to be proven. It is possible that the prevention of egg allergy requires a different approach by targeting microbial pathogens.
Keywords: Archaea, Bacteria, Skin, atopic dermatitis, cross-reactivity, egg allergy, IgE sensitization
Received: 24 Jul 2019;
Accepted: 04 Nov 2019.
Copyright: © 2019 Ong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Peck Ong, Children's Hospital of Los Angeles, Division of Clinical Immunology and Allergy, Los Angeles, United States, firstname.lastname@example.org