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Intestinal barrier dysfunction and food allergy

Rivista di immunologia ed allergologia pediatrica. 2024 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 45 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Edited by the SIAIP Food Allergy Commission, Caterina Anania, Barbara Cuomo, Enza D’Auria, Fabio Decimo, Giovanni Cosimo Indirli, Enrica Manca, Filippo Mondì, Erica Pendezza, Marco Ugo Andrea Sartorio, Mauro Calvani

Summary

This review applies the epithelial barrier hypothesis to food allergy, arguing that environmental exposures including microplastics, nanoplastics, food additives, and detergents disrupt gut and skin barriers and drive the rise in allergic disease.

The dramatic increase in allergic diseases has been explained by different hypotheses over time. Most recently, the epithelial barrier hypothesis argues that environmental exposure to toxic substances (detergents, microplastics and nanoplastics, food additives such as enzymes and emulsifiers), a consequence of the modern lifestyle, damage the epithelial barrier of the skin, airways, and intestinal mucosa leading to the onset of various diseases including food allergy. Numerous studies have shown a link between increased intestinal permeability and food allergy. Increased intestinal permeability, by facilitating exposure to allergens, triggers the activation of an immune response involving epithelial cells and immune cells and causes an abnormal Th2-type response. A key role is also played by the gut microbiota and ultimately by diet in determining the proper functioning of this barrier. Opportunities for intervention to repair the damage of the epithelial barrier at present consist of the use of certain components of the diet such as small peptides contained within hydrolyzed formulas, prebiotics, probiotics, vitamins, and fiber that can positively influence barrier function by acting directly on the integrity of the barrier itself, or indirectly through modulation of the gut microbiota. Other strategies such as microRNAs, small molecules, and transplantation of the gut microbiota are under investigation.

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