Food Allergy and the Oral Immunotherapy Approach

Cabrera, Carmen; Urra, José Miguel

doi:10.1007/s00005-014-0304-z

Cited by 15 publications

(7 citation statements)

References 80 publications

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“…In our study, gut microbiota dysbiosis reduced the level of TJs (ZO-1, Occludin, claudin-1), resulting in the damage of tight junction colonization and increased intestinal permeability. The initiation of food allergies may require disturbances in the local microenvironment in order to prevent tolerance [63]. Our research supports this point, and this may also be why gut microbiota dysbiosis caused by antibiotics increases the susceptibility and severity of food allergies.…”

Section: Discussionsupporting

confidence: 78%

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

et al. 2021

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(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

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Section: Discussionsupporting

confidence: 78%

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

et al. 2021

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“…It has been proposed that, as in tolerance, the main mechanism underlying OIT is induction of Tregs with concomitant increases in IL-10 and TGF- β . 38 However, there is no conclusive evidence of this in humans, and it is as yet unclear whether a waning of allergic sensitization, an induction of Tregs, or other factors cause tolerance. 39,40 …”

Section: Immunotherapy: Cellular and Molecular Responses And Potentiamentioning

confidence: 99%

Deciphering the black box of food allergy mechanisms

Sampath

Tupa

Graham

et al. 2017

Annals of Allergy, Asthma & Immunology

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Objective To review our current understanding of immunotherapy, the immune mechanisms underlying food allergy, and the methodological advances that are furthering our understanding of the role of immune cells and other molecules in mediating food allergies. Data Sources Literature searches were performed using the following combination of terms: allergy, immunotherapy, food, and mechanisms. Data from randomized clinical studies using state-of-the-art mechanistic tools were prioritized. Study Selections Articles were selected based on their relevance to food allergy. Results Current standard of care for food allergies is avoidance of allergenic foods and the use of epinephrine in case of severe reaction during unintentional ingestion. During the last few decades, great strides have been made in understanding the cellular and molecular mechanisms underlying food allergy, and this information is spearheading the development of exciting new treatments. Conclusion Immunotherapy protocols are effective in desensitizing individuals to specific allergens; however, recurrence of allergic sensitization is common after discontinuation of therapy. Interestingly, in a subset of individuals, immunotherapy is protective against allergens even after discontinuation of immunotherapy. Whether this protection is permanent is currently unknown because of inadequate long-term follow-up data. Research on understanding the underlying mechanisms may assist in modifying protocols to improve outcome and enable sustained unresponsiveness, rather than a temporary relief against food allergies. The cellular changes brought about by immunotherapy are still a black box, but major strides in our understanding are being made at an exciting pace.

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“…Increase in Foxp3 + CD4 + Tregs has been linked to inhibition of FAs initiated by Th2-related cytokines such as IL-4, IL-5, and IL-13 [ 38 – 40 ]. In this study, PCB extract administration significantly promoted oral tolerance via the generation of Foxp3 + Tregs and suppressed OVA-induced Th2-dominant immune responses in FA.…”

Section: Discussionmentioning

confidence: 99%

Regulatory T Cell Induced byPoria cocosBark Exert Therapeutic Effects in Murine Models of Atopic Dermatitis and Food Allergy

Bae

See

Choi

et al. 2016

Mediators of Inflammation

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The prevalence of allergic disorders including atopic dermatitis (AD) and food allergy (FA) has increased dramatically in pediatric populations, but there is no effective drug available for their management. Therefore, trials are required for the development of safe therapeutic agents such as herbal medicines. We determined whether orally administered Poria cocos bark (PCB) extract could exert immunosuppressive effects on allergic and inflammatory symptoms of AD and FA. For both AD, which was induced using house dust mite extract, and FA, which was induced by exposure to ovalbumin, model mice were orally treated with PCB extract for 62 days and 18 days, respectively. We also investigated the inductive effect of PCB extract on the generation and maintenance of Foxp3+CD4+ regulatory T cells (Tregs). The symptoms of AD and FA were ameliorated by the administration of PCB extract. Furthermore, PCB extract inhibited the Th2-related cytokines and increased the population of Foxp3+CD4+ Tregs in both AD and FA models. In ex vivo experiments, PCB extract promoted the functional differentiation of Foxp3+CD4+ Tregs, which is dependent on aryl hydrocarbon receptor activation. Thus, PCB extract has potential as an oral immune suppressor for the treatment of AD and FA through the generation of Tregs.

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Food Allergy and the Oral Immunotherapy Approach

Cited by 15 publications

References 80 publications

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

Deciphering the black box of food allergy mechanisms

Regulatory T Cell Induced byPoria cocosBark Exert Therapeutic Effects in Murine Models of Atopic Dermatitis and Food Allergy

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