Multifactorial Modulation of Food-Induced Anaphylaxis

Abstract

Prevalence of food-induced anaphylaxis increases progressively and occurs in an unpredictable manner, seriously affecting the quality of life of patients. Intrinsic factors including age, physiological, and genetic features of the patient as well as extrinsic factors such as the intake of drugs and exposure to environmental agents modulate this disorder. It has been proven that diseases, such as mastocytosis, defects in HLA, or filaggrin genes, increase the risk of severe allergic episodes. Certain allergen families such as storage proteins, lipid transfer proteins, or parvalbumins have also been linked to anaphylaxis. Environmental factors such as inhaled allergens or sensitization through the skin can exacerbate or trigger acute anaphylaxis. Moreover, the effect of dietary habits such as the early introduction of certain foods in the diet, and the advantage of the breastfeeding remain as yet unresolved. Interaction of allergens with the intestinal cell barrier together with a set of effector cells represents the primary pathways of food-induced anaphylaxis. After an antigen cross-links the IgEs on the membrane of effector cells, a complex intracellular signaling cascade is initiated, which leads cells to release preformed mediators stored in their granules that are responsible for the acute symptoms of anaphylaxis. Afterward, they can also rapidly synthesize lipid compounds such as prostaglandins or leukotrienes. Cytokines or chemokines are also released, leading to the recruitment and activation of immune cells in the inflammatory microenvironment. Multiple factors that affect food-induced anaphylaxis are discussed in this review, paying special attention to dietary habits and environmental and genetic conditions.

Microbial signature in IgE-mediated food allergies

“…The cause for different relative abundance of P. copri in the different FAs is not fully understood and might be explained by a variety of known allergen-related risk factors: genetic, environmental, or dietary habits, such as lack of breastfeeding and a low-fiber diet [ 47 ]. Further research needs to be carried out in order to elucidate the contribution of different factors to the different abundances of P. copri in FAs and its effects on the FA disease state.…”

Skin, gut, and lung barrier: Physiological interface and target of intervention for preventing and treating allergic diseases

“…55 Following sensitization, subsequent exposure to the allergen triggers IgE-mediated release of preformed inflammatory mediators, such as histamine or heparin, from mast cells. 56 Rapid synthesis and release of lipid mediators (leukotrienes, platelet-activating factor, and prostaglandins) and the production of cytokines by activated mast cells follows. In genetically predisposed individuals, similar immunological pathways can be activated in the absence of an IgE-mediated reaction.…”

“…IL‐25 drives activation of IL‐5/IL‐13‐secreting ILC2s in the intestine, increasing mast cell numbers and intestinal permeability 55 . Following sensitization, subsequent exposure to the allergen triggers IgE‐mediated release of preformed inflammatory mediators, such as histamine or heparin, from mast cells 56 . Rapid synthesis and release of lipid mediators (leukotrienes, platelet‐activating factor, and prostaglandins) and the production of cytokines by activated mast cells follows.…”

Personalized Nutrition Approach in Food Allergy: Is It Prime Time Yet?

“…Different geographical locations show some differences in food allergen triggers for anaphylaxis. A recent one from Spain suggested milk and eggs allergies are more severe than nuts in their population [ 13 ].…”