Maternal allergy increases susceptibility to offspring allergy in association with TH2-biased epigenetic alterations in a mouse model of peanut allergy

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Background: Food allergy research is hampered by a lack of animal models that consistently mimic human food allergic responses. Laboratory mice are generally fed grain-based chow made with large amounts of soybeans rich in immunomodulatory isoflavones. We tested the role of dietary soy components in the induction of food allergic responses in the BALB/c mouse strain, which is known to be resistant to anaphylaxis when orally challenged by food allergens. Methods: Mice were fed a soy-free diet for 2 generations. After weaning, mice were maintained on the same diet or fed a diet containing soy isoflavones, i.e. genistein and daidzein, followed by weekly oral sensitizations with crude peanut extract plus cholera toxin and finally challenged at week 7. The anaphylactic symptoms, body temperature, peanut-specific antibodies and mast cell degranulation were assessed. Results: Soy-free diet mice showed significantly higher anaphylactic symptom scores and mast cell degranulation after challenge and higher peanut-specific antibody levels than mice fed regular chow. Introduction of a regular soy diet or an isoflavone diet to soy-free diet mice significantly suppressed the allergic reactions compared to the soy-free diet. Conclusion: Rodent diet is an important variable and needs to be taken into consideration when designing experiments involving animal models. Our results indicate that elimination of soy components from the diet enhances peanut sensitization in BALB/c mice. In addition to serving as a valuable tool to mimic human food allergy, the dietary influence on the immune response could have far-reaching consequences in research involving animal models.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dietary Elimination of Soybean Components Enhances Allergic Immune Response to Peanuts in BALB/c Mice

Chang¹,

Song²,

Li³

et al. 2015

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“…Studies have also shown that antenatal particulate exposure in mice resulted in distinct methylation changes and increased susceptibility to allergic airway diseases in up to three subsequent offspring generations [92, 93]. In a murine model of peanut allergy, offspring of peanut-sensitized mothers were more susceptible to the development of peanut allergy, through epigenetic alterations of the IL-4 gene promoter [94]. …”

Section: Second-generation International Immigrantsmentioning

confidence: 99%

Effects of Migration on Allergic Diseases

Tham

Zhu

2018

Studies in migrant populations provide vital opportunities to investigate the role of environmental factors in the pathogenesis of allergic disorders. Differences in allergy prevalence have been observed between migrants and native-born subjects living in the same geographical location. Immigrants who migrate from less affluent countries with lower allergy prevalence tend to have a lower prevalence of allergic disorders compared to native-born residents of the more affluent host country. The patterns of allergic disease prevalence also differ between first- and second-generation migrants. The timing of migration in relation to birth, age at migration, and duration of residence in the host country also influence one’s atopic risk. A complex interplay of multiple environmental, socioeconomic, and cultural factors is likely responsible for these observed differences. Further research into the roles of various risk factors in modulating differences in allergic disease prevalence between migrant and native populations will enhance our understanding of the complex gene-environment interactions involved in the pathogenesis of allergic disorders.

“…Song et al [21] conducted an animal (mouse) study in order to examine the relationship of allergy susceptibility and Th2-biased epigenetic alterations. The offspring of mothers with peanut allergy and the offspring of naive mothers were both sensitized with peanut.…”

Section: Interleukinsmentioning

confidence: 99%

The Implications of DNA Methylation on Food Allergy

Lee

Song

O’Sullivan

et al. 2017

Food allergy is a major clinical and public health concern worldwide. The risk factors are well defined, however, the mechanisms by which they affect immune development remain largely unknown, and unfortunately the effective treatment or prevention of food allergy is still being researched. Recent studies show that the genes that are critical for the development of food allergy are regulated through DNA methylation. Environmental factors can affect host DNA methylation status and subsequently predispose people to food allergy. DNA methylation is therefore an important mediator of gene-environment interactions in food allergy and key to understanding the mechanisms underlying the allergic development. Indeed, the modification and identification of the methylation levels of specific genetic loci have gained increasing attention for therapeutic and diagnostic application in combating food allergy. In this review, we summarize and discuss the recent developments of DNA methylation in food allergy, including the pathogenesis, therapy, and diagnosis. This review will also summarize and discuss the environmental factors that affect DNA methylation levels in food allergy.