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Research Article | Open Access | Just Accepted

High-fat diet aggravates food allergy via the microbiota-intestinal epithelium interactions: a review

Xumei Wanga,bHui WangcYanhong Shaoa,bJun Liua,b ( )Zongcai Tua,b,c ( )

Abstract

The rising incidence of food allergy attracts researchers to advocate that a high-fat diet (HFD) is an attention-grabbing trigger. However, the mechanism by which HFD aggravates food allergy remains largely unknown. In this context, intestinal epithelium dysfunction as a characteristic of food allergy is summarized. Specifically, we focus our attention on the microbiota-intestinal epithelium interactions and call attention to the underlying mechanism by which HFD promotes food allergy along the interactions. Escaped fat and excessed bile acids in the colon induced by HFD can disrupt gut microbiota, directly regulating intestinal epithelium function. Additionally, HFD contributes to indirectly destroying the intestinal epithelium and enhancing its permeability by altering the level of microbial metabolites. Consequently, these ways promote the influx of food allergens. Substantial quantities of food allergens traverse the intestinal epithelium, prompting heightened secretion of pro-inflammatory cytokines, thus favoring a Th2 immune response. In this situation, impaired differentiation of Treg and Th1 cells can aggravate food allergy. Clarifying the intricate relationship between HFD and food allergy from the microbiota-intestinal epithelium interactions may offer prevention strategies for food allergy.

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Food Science and Human Wellness

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Cite this article:
Wang X, Wang H, Shao Y, et al.

High-fat diet aggravates food allergy via the microbiota-intestinal epithelium interactions: a review. Food Science and Human Wellness, 2025, https://doi.org/10.26599/FSHW.2025.9250578

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Received: 16 December 2024
Revised: 07 January 2025
Accepted: 11 February 2025
Available online: 22 March 2025

© 2025 Beijing Academy of Food Sciences. Publishing services by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).