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Pollen-Food Allergy Syndrome: A not so Rare Disease in Childhood

Mastrorilli, Carla, Cardinale, Fabio, Giannetti, Arianna, Caffarelli, Carlo·2019·Medicina
DOI 10.3390/medicina55100641PMC PMC6843262
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Abstract

Seasonal allergic rhinoconjunctivitis (SAR) affects millions of people worldwide, particularly in childhood and adolescence. Pollen food allergy syndrome (PFAS) is a common adverse reaction occurring few minutes after the consumption of vegetable foods in patients with pollen-induced SAR. PFAS has rarely been investigated in the pediatric population, as it has been mainly examined as an adult disease. Recent studies suggested that PFAS might be more frequent in childhood than previously recognized. The present review aims to give an overview of the epidemiology, pathophysiology, diagnosis, management and prognosis of PFAS in children with SAR-induced by pollens.

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Figure 1 Time course, pathogenesis, and manifestations of pollen-food allergy syndrome. (A) Preliminar phase: Sensitization to pollen. Airborne allergen contact via the respiratory tract activates, after processing by antigen presenting cells (APC), such as dendritic cell, naïve T helper cells with the antigen-specific receptors. In allergic sensitization the differentiation leans towards the TH2 phenotype, with the release of interleukins 4, 5, and 13. Eosinophils are recruited and activated by IL-5. The production of antigen-specific IgEs through B cells (primary sensitization) are stimulated by IL-4 and IL-13. (B) Clinical phase: Plant-derived food reactions. Ingestion of cross-reacting molecules induces the secondary immune response via T-cell and IgE memory. The degranulation of mast cells leads to the release of granules of preformed inflammatory mediators (e.g., histamine) and the de novo synthesis and/or release of inflammatory mediators (e.g., Leukotrienes), proteases (e.g., Tryptase), cytokines (e.g., IL-4) and chemotactic molecules. Allergic symptoms occur shortly after ingestion in the locations of the contact to the allergen (e.g., mouth, throat, intestine) or in the organs (systemic symptoms). IgE, immunoglobulin E; IL, interleukin.
Figure 1 Time course, pathogenesis, and manifestations of pollen-food allergy syndrome. (A) Preliminar phase: Sensitization to pollen. Airborne allergen contact via the respiratory tract activates, after processing by antigen presenting cells (APC), such as dendritic cell, naïve T helper cells with the antigen-specific receptors. In allergic sensitization the differentiation leans towards the TH2 phenotype, with the release of interleukins 4, 5, and 13. Eosinophils are recruited and activated by IL-5. The production of antigen-specific IgEs through B cells (primary sensitization) are stimulated by IL-4 and IL-13. (B) Clinical phase: Plant-derived food reactions. Ingestion of cross-reacting molecules induces the secondary immune response via T-cell and IgE memory. The degranulation of mast cells leads to the release of granules of preformed inflammatory mediators (e.g., histamine) and the de novo synthesis and/or release of inflammatory mediators (e.g., Leukotrienes), proteases (e.g., Tryptase), cytokines (e.g., IL-4) and chemotactic molecules. Allergic symptoms occur shortly after ingestion in the locations of the contact to the allergen (e.g., mouth, throat, intestine) or in the organs (systemic symptoms). IgE, immunoglobulin E; IL, interleukin.CC BY · PubMed Central

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Metadata

Authors
Mastrorilli, C., Cardinale, F., Giannetti, A., & Caffarelli, C.
Venue
Medicina
Publisher
MDPI AG
Published
2019-09-26
Volume
55
Issue
10
Pages
641
ISSN
1648-9144
DOI
10.3390/medicina55100641
PMC
PMC6843262
Cited by
78
References
3
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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