Dysbiosis in food allergy and implications for microbial therapeutics.
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ABSTRACT:
SUBMITTER: Berin MC
PROVIDER: S-EPMC7810494 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The prevalence of IgE mediated food allergy is an increasing public health concern. The current standard of treatment is strict avoidance of the offending food(s). There are no FDA approved treatments for food allergy. This review will provide an overview of strategies currently under investigation for the treatment of food allergy. The main focus of research has been directed at various forms of immunotherapy, including oral, sublingual and epicutaneous delivery routes. While oral immunotherapy (OIT) has shown the greatest promise for efficacy in terms of amount of protein that can be ingested, it has also demonstrated less tolerability and a less favorable safety profile as compared to sublingual immunotherapy (SLIT) and epicutaneous immunotherapy (EPIT), which offers the least protection but has the best safety and tolerability profile. Investigation is also underway for modified antigens that may be used for immunotherapy and for adjuncts that may help facilitate immunotherapy, including biologics such as anti-IgE therapy, and also probiotics. There are also a number of preclinical concepts that are being evaluated to manipulate the antigens and/or the immune system that may one day be translatable to patients.
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Project description:Food allergy is a life-threatening response to specific foods, and microbiota imbalance (dysbiosis) in gut is considered a cause of this disease. Meanwhile, the host immune response also plays an important role in the disease. Notably, interleukin 33 (IL-33) released from damaged or necrotic intestinal epithelial cells facilitates IL-2-producing CD4 helper T (Th2) responses. However, causal relationships between the gut and oral dysbiosis and food allergy remain unknown. In this study, we analyzed effects of gut and oral dysbiosis on development of food allergy. A murine model of food allergy was established via ovalbumin (OVA) injection in BALB/c mice. Viable fecal bacteria were identified using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS). il33 expression in colon-26 mouse colon cells stimulated by isolated fecal bacteria was quantified by real-time PCR. Intestinal T cells from the mice were analyzed by flow cytometry. Salivary IgA levels were quantified by enzyme-linked immunosorbent assay (ELISA), and IgA-bound oral bacteria were detected by flow cytometry. Among fecal bacteria, the abundance of Citrobacter sp. increased in the feces of allergic mice and induced il33 expression in colon-26 cells. Orally administered Citrobacter koseri JCM1658 exacerbated systemic allergic symptoms and reduced intestinal Th17 cells. Salivary IgA and IgA-bound oral bacteria increased in the allergic mice. Based on the results described above, food allergy induced both gut and oral dysbiosis. Citrobacter sp. aggravated allergy symptoms by inducing IL-33 release from intestinal epithelial cells.
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Project description:Food allergies affect up to 6% of young children and 3%-4% of adults. They encompass a range of disorders that may be IgE and/or non-IgE mediated, including anaphylaxis, pollen food syndrome, food-protein-induced enterocolitis syndrome, food-induced proctocolitis, eosinophilic gastroenteropathies, and atopic dermatitis. Many complex host factors and properties of foods are involved in the development of food allergy. With recent advances in the understanding of how these factors interact, the development of several novel diagnostic and therapeutic strategies is underway and showing promise.
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Project description:Although the anti-allergic and prebiotic activities of diosgenin have been reported, the influence of diosgenin on intestinal immune and epithelial cells remains unclear. As the gut microbiota plays an important role in allergic disorders, this study aimed to investigate whether the anti-allergic diarrhea effect of diosgenin occurs via improving gut dysbiosis. In a murine food allergy model, the density of fecal bacterial growth on de Man, Rogossa and Sharpe (MRS) plates was diminished, and growth on reinforced clostridial medium (RCM) and lysogeny broth (LB) agar plates was elevated. However, the oral administration of diosgenin reduced the density of fecal bacteria and ameliorated diarrhea severity. Concordantly, reshaped diversity and an abundance of fecal microbes were observed in some of the diosgenin-treated mice, which showed a milder severity of diarrhea. The relevant fecal strains from the diosgenin-treated mice were defined and cultured with Caco-2 cells and allergen-primed mesenteric lymph node (MLN) cells. These strains exhibited protective effects against the cytokine/chemokine network and allergen-induced T-cell responses to varying degrees. By contrast, diosgenin limitedly regulated cytokine production and even reduced cell viability. Taken together, these findings show that diosgenin per se could not directly modulate the functionality of intestinal epithelial cells and immune cells, and its anti-allergic effect is most likely exerted via improving gut dysbiosis.
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Project description:Background: Although adverse food reactions are commonly divided into immunoglobulin E (IgE) mediated food allergy (FA), and non-IgE FA, the current literature is providing support for the role of innate immune responses as an important component of non-IgE FA. Using a commercially available leukocyte activation (LA) assay, a recent quantitative study of total extracellular DNA released in cellular supernatants of human peripheral blood mononuclear cells exposed either to positive or negative tested foods demonstrated that leukocytes exposed to foods with positive LA test results showed higher DNA content than those exposed to foods with negative LA test results. In humans, the origin of DNA might be either the nucleus or the mitochondria. Analysis of emerging data from several laboratories, including our own, suggests that mitochondrial DNA induces inflammatory responses through induction of proinflammatory cytokines. Objective: This pilot study was designed primarily to convey the finding, and relevance of, mitochondrial DNA in the form of neutrophil extracellular traps (NET) as a new pathogenetic mechanism for innate immune-mediated non-IgE FA. Methods: The study population consisted of a total of six subjects, four in a major FA study group and two in a subgroup. Neutrophils were isolated and treated with food antigens that elicited positive and negative LA responses, and the released free DNA was analyzed for the cellular site of origin by using real-time polymerase chain reaction and for leukocyte calprotectin and S100 calcium-binding protein A12 (S100A12) proteins as markers of NETs. Results: We showed that cellular supernatants from neutrophils treated with foods that elicit positive LA responses can contain increased DNA levels of nuclear as well as mitochondrial origin. Supernatants from neutrophils treated with negative tested food (LA) responses did not induce the release of nuclear or mitochondrial DNA. Conclusion: Analysis of our data suggested that the induction of NETs that contain proinflammatory mitochondrial DNA may provide the critical link necessary for a better understanding of the pathogenesis of non-IgE-mediated FA. These discoveries may not only facilitate better diagnostic tests of FA but should also improve clinical management of allergic and other inflammatory diseases.
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