Ingestion Of Allergen Research Articles

Oral administration of egg ovalbumin allergen induces dysregulation of tryptophan metabolism in sensitized BALB/c mice.

Food allergy (FA), triggered by specific dietary allergens, has emerged as a substantial global concern for food safety and public health. While studies have elucidated changes in immune cells and cytokines associated with allergen exposure, a comprehensive analysis of the host's metabolic features and the interaction between metabolites and the gut microbiota has not been conducted. In this study, egg allergen ovalbumin (OVA) was administered by the oral route to sensitized BALB/c mice to faithfully replicate key aspects of human FA, including severe allergic diarrhea, mast cell infiltration, and elevated levels of serum IgE, mMCPT-1, and Th2 cell hallmark cytokines (such as IL-4, IL-5, and IL-13). Furthermore, the untargeted and targeted metabolomic analyses indicated that FA in mice precipitated a substantial decrease in the tryptophan metabolites indole-3-acrylic acid (IA) and indole-3-lactic acid (ILA). The integration of shotgun metagenome and metabolome data further unveiled that the dysregulation of indole metabolism is related to a decline in the abundance of beneficial bacteria such as Lactobacillus and Bifidobacterium. Additionally, disruption of the tryptophan indole derivative pathway compromises the maintenance of intestinal mucosal function through the AHR signaling pathway, manifested by decreased expression of Reg3g and IL22. Taken together, this study demonstrated that the anaphylaxis triggered by oral ingestion of food allergens can lead to disruptions in tryptophan metabolism, consequently impairing intestinal immune homeostasis.

History and physycal examination

The most effective method for diagnosing food allergy is the clinical history, which includes anamnesis and physical examination. The anamnesis must include a directed and detailed questioning, and together with the physical examination, it will provide the necessary data to guide the diagnosis and suggest whether the pathophysiology is mediated or not by IgE, which is relevant for the selection and interpretation of the tests. specific and establish the accurate diagnosis, in addition to evaluating the possibility of distinguishing between the different differential diagnoses. It is important to assess the clinical history, because no in vivo or in vitro test is relevant if it is not confirmed with it. Even if there is a strong history of food allergy detected in the history, positive tests can confirm the diagnosis without the need for oral challenge, thus avoiding the risk and cost of performing it. The expression of food allergy is influenced by non-modifiable risk factors that include sex, race and genetics (familial), and modifiable factors: atopic dermatitis, vitamin D deficiency, diet high in polyunsaturated fats and deficient in antioxidants, consumption of antacid drugs, obesity, increased hygiene, influence of the microbiota, time and route of food exposure (increased risk by delaying oral ingestion of allergens and concomitant environmental exposure of the same that leads to sensitization and allergy).

Epitope-Based IgE Assays and Their Role in Providing Diagnosis and Prognosis of Food Allergy.

With advances in molecular and computational science, epitope-specific IgE antibody profiling has been developed and recently brought into clinical practice. Epitope-based testing detects IgE antibodies that directly bind to antigenic sites of an allergen, providing increased resolution specificity and fewer false-positive results for diagnosing food allergy. Epitope-binding profiles may also serve as prognostic markers of food allergy and help predict quantities of allergen that would provoke a reaction (ie, eliciting dose, possible severity of a reaction after allergen ingestion, and outcomes of treatment options such as oral immunotherapy [OIT]). Future studies are under way to discover additional applications of epitope-specific antibodies for multiple food allergens.

Pediatric allergies in Japan: Coronavirus disease pandemic-related risk factors.

The coronavirus disease 2019 (COVID-19) pandemic impacted various parts of society, including Japanese children with allergies. This study investigated risk factors for pediatric allergic diseases associated with the state of emergency owing to the COVID-19 pandemic in Japan, including during school closures. Parents of pediatric patients (0-15 years) with allergies were enrolled and queried regarding the impact of school closure on pediatric allergies compared to that before the COVID-19 pandemic. A valid response was obtained from 2302 parents; 1740 of them had children with food allergies. Approximately 4% (62/1740) of the parents reported accidental food allergen ingestion was increased compared to that before the COVID-19 pandemic. Accidental ingestion during school closures was associated with increased contact with meals containing allergens meant for siblings or other members of the family at home. The exacerbation rate during the pandemic was highest for atopic dermatitis at 13% (127/976), followed by allergic rhinitis at 8% (58/697), and bronchial asthma at 4% (27/757). The main risk factors for worsening atopic dermatitis, allergic rhinitis, and bronchial asthma were contact dermatitis of the mask area (34/120 total comments); home allergens, such as mites, dogs, and cats (15/51 total comments); and seasonal changes (6/25 total comments), respectively. The main factors affecting allergic diseases were likely related to increased time at home, preventive measures against COVID-19, and refraining from doctor visits. Children with allergies were affected by changes in social conditions; however, some factors, such as preventing accidental ingestion and the management of allergens at home, were similar to those before the COVID-19 pandemic. Patients who had received instructions on allergen avoidance at home before the pandemic were able to manage their disease better even when their social conditions changed.

Immune sensing of food allergens promotes avoidance behaviour

In addition to its canonical function of protection from pathogens, the immune system can also alter behaviour1,2. The scope and mechanisms of behavioural modifications by the immune system are not yet well understood. Here, using mouse models of food allergy, we show that allergic sensitization drives antigen-specific avoidance behaviour. Allergen ingestion activates brain areas involved in the response to aversive stimuli, including the nucleus of tractus solitarius, parabrachial nucleus and central amygdala. Allergen avoidance requires immunoglobulin E (IgE) antibodies and mast cells but precedes the development of gut allergic inflammation. The ability of allergen-specific IgE and mast cells to promote avoidance requires cysteinyl leukotrienes and growth and differentiation factor 15. Finally, a comparison of C57BL/6 and BALB/c mouse strains revealed a strong effect of the genetic background on the avoidance behaviour. These findings thus point to antigen-specific behavioural modifications that probably evolved to promote niche selection to avoid unfavourable environments.

Perspectives on Non-IgE-Mediated Gastrointestinal Food Allergy in Pediatrics: A Review of Current Evidence and Guidelines.

Food allergy is an immune-mediated disease that can result in considerable morbidity and even mortality, with a significant negative impact on patients' quality of life. It is characterized by allergic symptoms that can occur shortly after a relevant food allergen ingestion, or can be delayed or chronic, which make it more difficult for diagnosis. The symptoms of this disease can range from mild to severe, and rarely can cause anaphylaxis, a life-threatening allergic reaction. The prevalence of non-immunoglobulin E (IgE)-mediated food allergy is poorly established outside of cow's milk allergy, with an adjusted incidence ranging between 0.13% and 0.72%. Several disorders are classified as non-immunoglobulin E (IgE)-mediated food allergies that predominantly affect the gastrointestinal tract including food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP), food protein-induced allergic enteropathy (FPE), and food protein-induced dysmotility disorders (GORD and constipation). Eosinophilic esophagitis (EoE) is listed in this group, even though it considered by some authorities to be mixed reaction with both IgE and cell-mediated immune response to be involved in the reaction. The most common types of non-IgE-mediated food allergy are food protein-induced enterocolitis syndrome (FPIES) and food protein-induced allergic proctocolitis (FPIAP). These disorders typically present in infancy and are often triggered by cow's milk protein. Patients with FPIES present with profuse emesis and dehydration, while FPIAP patients present with hematochezia in otherwise healthy infants. Since there are no specific confirmatory non-invasive diagnostic laboratory tests, the diagnosis is usually made clinically when typical symptoms improve upon the removal of the culprit food. Food reintroduction should be attempted, when possible, with documentation of symptoms of relapse to confirm the diagnosis. The management includes dietary avoidance, supportive treatment in the case of accidental exposure, and nutritional counseling. This review focuses on the clinical manifestations, epidemiology, management, and recent guidelines of the most common non-IgE-mediated food hypersensitivity disorders (FPIES, FPIAP, and FPE).

Systemic contact dermatitis to peanut ingestion

Delayed cutaneous hypersensitivity with ingestion of allergen (a form of systemic contact dermatitis) involves a non-cutaneous exposure to an allergen that has already been sensitized through the cutaneous route.1 The exact mechanism for systemic contact dermatitis remains unclear, but is believed to be mediated by type IV hypersensitivity involving T-cell activation to a hapten. 1 Ingestion of Balsam of Peru and nickel are most frequently implicated in systemic contact dermatitis, with Balsam of Peru commonly found in citrus fruits, tomatoes, and spices, and nickel commonly found in grains, chocolate, and canned foods.

A pragmatic approach to infant feeding for food allergy prevention.

Early introduction of allergenic foods into an infant's diet is currently the most promising strategy to prevent food allergy, with infant guidelines around the world shifting from promoting avoidance to actively encourage the introduction of allergenic foods in the infant diet. Infant feeding guidelines vary according to regional public health priorities, and knowledge gaps remain, resulting in ongoing challenges for clinicians and families to translate guidelines into practical strategies for the introduction of complementary foods for food allergy prevention. Evidence from Australia demonstrates high community support and uptake of revised guidelines with most parents introducing allergenic foods in the first year of life, although this has not had the expected impact on substantially reducing food allergy prevalence. To uptake of guidelines from other countries is less clear, and several barriers have been noted in infant feeding RCTs, which may warrant intervention strategies. Further research is needed to understand additional strategies for food allergy prevention, particularly in infants who develop food allergy prior to when they are developmentally ready to commence solids. Several RCTs are underway investigating preventative strategies that target the window before allergen ingestion, such as vitamin D supplementation, emollient use, and immunizations that prime the immune response away from a Th2‐driven allergic phenotype. Further research is also needed to understand the role of the environment and the host environment in the development of tolerance to foods.

Tree Nuts and Peanuts as a Source of Beneficial Compounds and a Threat for Allergic Consumers: Overview on Methods for Their Detection in Complex Food Products.

Consumption of tree nuts and peanuts has considerably increased over the last decades due to their nutritional composition and the content of beneficial compounds. On the other hand, such widespread consumption worldwide has also generated a growing incidence of allergy in the sensitive population. Allergy to nuts and peanuts represents a global relevant problem, especially due to the risk of the ingestion of hidden allergens as a result of cross-contamination between production lines at industrial level occurring during food manufacturing. The present review provides insights on peanuts, almonds, and four nut allergens—namely hazelnuts, walnuts, cashew, and pistachios—that are likely to cross-contaminate different food commodities. The paper aims at covering both the biochemical aspect linked to the identified allergenic proteins for each allergen category and the different methodological approaches developed for allergens detection and identification. Attention has been also paid to mass spectrometry methods and to current efforts of the scientific community to identify a harmonized approach for allergens quantification through the detection of allergen markers.

Exploring the impacts of FDA temporary food labeling flexibility among the food allergy community during the Covid-19 pandemic

ABSTRACT In an attempt to improve access to food distribution systems during the Covid-19 pandemic, the United States Food and Drug Administration (FDA) issued temporary flexibility in food labeling requirements. This requirement affects the Top 8 allergens and could lead to accidental allergen ingestion. The purpose of this study was to utilize a qualitative method to collect and analyze comments to FDA that were available via Allergic Living’s website from May 22, 2020, to June 18, 2020, following the release of the food labeling change. In total, 3,033 comments were analyzed using the thematic analysis six-phase framework approach. Various themes were extracted relating to the emotional responses of the new labeling including fear, safety concerns, and trust of certain food product brands among the food allergy community. This research has implications for a broad spectrum of the U.S. food industry including restaurants, grocery stores, specialty food associations, and consumers. Stakeholders and experts in the food allergy community should be consulted when a policy change is occurring, especially during a pandemic affecting access to safe food.

Separating Fact from Fiction in the Diagnosis and Management of Food Allergy

Separating Fact from Fiction in the Diagnosis and Management of Food Allergy

Safety of repetitive ingestion of food allergen at home after mild symptoms during oral food challenge

Safety of repetitive ingestion of food allergen at home after mild symptoms during oral food challenge

Can food allergy be cured? What are the future prospects?

Food allergies have become a significant heath burden as prevalence continues to rise, affecting 6%-13% of the global population. In the absence of drugs approved by regulatory agencies, the current standard of care remains avoidance of allergenic foods and management of acute allergic reactions with antihistamines and epinephrine autoinjectors. Allergen immunotherapy has been shown to increase the threshold of reactivity in the majority of food-allergic individuals. However, challenges include long treatment periods, high rates of adverse reactions, and lack of permanence of desensitization and established protocols. To address these limitations, adjunctive allergen-specific immunotherapy, vaccines, and non-allergen-specific therapies (eg, monoclonal antibodies) are being explored. The future of food allergy treatment is promising with a number of clinical trials in progress. Currently, although desensitization can be achieved for the majority of individuals with food allergy through immunotherapy, continued ingestion of allergen is needed for most individuals to maintain desensitization. Further understanding of the mechanisms of food allergy and identification of biomarkers to distinguish between temporary and permanent resolution of allergies is needed before a cure, where reactivity to the allergen is permanently lost enabling the individual to consume the allergen in any amount at any time, can be envisioned.

Chitinases as Food Allergens.

Food allergies originate from adverse immune reactions to some food components. Ingestion of food allergens can cause effects of varying severity, from mild itching to severe anaphylaxis reactions. Currently there are no clues to predict the allergenic potency of a molecule, nor are cures for food allergies available. Cutting-edge research on allergens is aimed at increasing information on their diffusion and understanding structure-allergenicity relationships. In this context, purified recombinant allergens are valuable tools for advances in the diagnostic and immunotherapeutic fields. Chitinases are a group of allergens often found in plant fruits, but also identified in edible insects. They are classified into different families and classes for which structural analyses and identification of epitopes have been only partially carried out. Moreover, also their presence in common allergen databases is not complete. In this review we provide a summary of the identified food allergenic chitinases, their main structural characteristics, and a clear division in the different classes.

Immunoglobulin E blockade during food allergen ingestion enhances the induction of inhibitory immunoglobulin G antibodies

Immunoglobulin E (IgE)-mediated food allergy is a growing problem with no curative therapy. 1 Renz H. Allen K.J. Sicherer S.H. et al. Food allergy. Nat Rev Dis Primers. 2018; 4: 17098 Crossref PubMed Scopus (179) Google Scholar Oral immunotherapy (OIT) has shown promise, but its utility is limited by reactions during treatment and a lack of sustained protection after therapy. Immunoglobulin E antibodies trigger hypersensitivity reactions to foods. Their effects, mediated by the high-affinity Immunoglobulin E receptor (FcεRI) on mast cells and basophils, can be countered by IgG antibodies of shared specificity signaling via the inhibitory Fc receptor, FcγRIIb. 2 Malbec O. Daeron M. The mast cell IgG receptors and their roles in tissue inflammation. Immunol Rev. 2007; 217: 206-221 Crossref PubMed Scopus (116) Google Scholar Oral immunotherapy induces only modest reductions in specific IgE antibodies but stimulates dramatic increases in inhibitory IgG. 3 Burton O.T. Logsdon S.L. Zhou J.S. et al. Oral immunotherapy induces IgG antibodies that act through FcgammaRIIb to suppress IgE-mediated hypersensitivity. J Allergy Clin Immunol. 2014; 134: 1310-1317 Abstract Full Text Full Text PDF PubMed Scopus (120) Google Scholar , 4 Santos A.F. James L.K. Bahnson H.T. et al. IgG inhibits peanut-induced basophil and mast cell activation in peanut-tolerant children sensitized to peanut major allergens. J Allergy Clin Immunol. 2015; 135: 1249-1256 Abstract Full Text Full Text PDF PubMed Scopus (176) Google Scholar

Oral immunotherapy with the ingestion of house dust mite extract in a murine model of allergic asthma

BackgroundAllergen-specific immunotherapy (ASIT) has the potential to modify allergic diseases, and it is also considered a potential therapy for allergic asthma. House dust mite (HDM) allergens, a common source of airborne allergen in human diseases, have been developed as an immunotherapy for patients with allergic asthma via the subcutaneous and sublingual routes. Oral immunotherapy with repeated allergen ingestion is emerging as another potential modality of ASIT. The aim of this study was to evaluate the therapeutic efficacy of the oral ingestion of HDM extracts in a murine model of allergic asthma.MethodsBABL/c mice were sensitized twice by intraperitoneal injection of HDM extracts and Al(OH)3 on day 1 and day 8. Then, the mice received challenge to induce airway inflammation by intratracheal instillation of HDM extracts on days 29–31. The treatment group received immunotherapy with oral HDM extracts ingestion before the challenge. All the mice were sacrificed on day 32 for bronchoalveolar inflammatory cytokines, mediastinal lymph node T cells, lung histology, and serum HDM-specific immunoglobulins analyses.ResultsUpon HDM sensitization and following challenge, a robust Th2 cell response and eosinophilic airway inflammation were observed in mice of the positive control group. The mice treated with HDM extracts ingestion had decreased eosinophilic airway inflammation, suppressed HDM-specific Th2 cell responses in the mediastinal lymph nodes, and attenuated serum HDM-specific IgE levels.ConclusionsOral immunotherapy with HDM extracts ingestion was demonstrated to have a partial therapeutic effect in the murine model of allergic asthma. This study may serve as the basis for the further development of oral immunotherapy with HDM extracts in allergic asthma.

IgE promotes type 2 innate lymphoid cells in murine food allergy.

Mast cells serve an important sentinel function at mucosal barriers and have been implicated as key early inducers of type 2 immune responses in food allergy. The generation of Th2 and IgE following food allergen ingestion is inhibited in the absence of mast cells. Group 2 innate lymphoid cells are also thought to play an important early role in nascent allergic responses. To test whether IgE-mediated mast cell activation promotes intestinal ILC2 responses following ingestion of food allergens and whether ILC2 amplify food allergy. Two different mouse models of food allergy, one using intraperitoneally ovalbumin (OVA)-primed BALB/c animals and the other using enterally peanut-sensitized inherently atopic IL4raF709 mice, were applied to test the contributions of IgE antibodies and mast cells to ILC2 responses. The effect of ILC2 on mast cell activation and on anaphylaxis was tested. ILC2 responses were significantly impaired in both models of food allergy in Igh7-/- mice harbouring a targeted deletion of the gene encoding IgE. A similar reduction in food allergen-induced ILC2 was observed in mast cell-deficient Il4raF709 KitW-sh mice, and this was partially corrected by reconstituting these animals using cultured bone marrow mast cells. Mast cells activated ILC2 for IL-13 production in an IL-4Rα-dependent manner. Activated ILC2 amplified systemic anaphylaxis by increasing target tissue sensitivity to mast cell mediators. These findings support an important role for IgE-activated mast cells in driving intestinal ILC2 expansion in food allergy and reveal that ILC2, in turn, can enhance responsiveness to the mediators of anaphylaxis produced by mast cells. Strategies designed to inhibit IgE signalling or mast cell activation are likely to inhibit both type 2 immunity and immediate hypersensitivity in food allergy.

Eating out with a food allergy in the UK: Change in the eating out practices of consumers with food allergy following introduction of allergen information legislation.

Strict allergen avoidance is important in day-to-day management of food allergy and avoidance when eating outside the home can present particular difficulties. EU legislation (EU FIC) introduced in December 2014 aimed to improve food allergen information provision for customers by requiring retailers of non-prepacked foods to provide information related to the content of one or more of 14 specified food allergens within their foods. To investigate the impact of EU FIC on the behaviours, experiences and attitudes of consumers with food allergy when eating out. As part of longitudinal research, participants with food allergy from across the UK took part in either (A) pre and post legislation in-depth interviews, or (B) pre and post legislation surveys. In-depth interviews were carried out with 28 participants pre and post legislation and analysed using the framework approach. Self-report surveys were completed by 129 participants pre and post legislation, and responses were subject to quantitative analyses. Improvements in allergen information provision and raised awareness of food allergy in eating out venues were reported following introduction of EU FIC. Whilst participants favoured written allergen information, they expressed greater confidence in communicating with eating out staff and in trusting the allergen information that they provided. Improvements were judged to be gradual, sporadic or inconsistent in implementation. For many participants, the "ideal" eating out experience was one in which a range of information resources were available and where written allergen information was complemented by proactive and accommodating staff within an allergy-aware environment. Whilst the onus is on legislators and food providers to ensure that adequate allergen information is provided, clinicians play an important role in encouraging patients with food allergy to pursue their legal right to make allergen enquiries to avoid accidental allergen ingestion when eating out.

Self-reported adverse food reactions and anaphylaxis in the SchoolNuts study: A population-based study of adolescents

Adolescents are at the highest risk of death from anaphylaxis, yet few population-based studies have described the frequencies and risk factors for allergic reactions caused by accidental allergen ingestion in this group. We describe the prevalence, frequency, and associated risk factors for recent adverse food reactions in 10- to 14-year-olds in Melbourne, Australia, recruited from a stratified, random, population-based sample of schools (SchoolNuts, n=9663; 48% response rate). Self-reported food allergy and adverse reaction details, including anaphylaxis, were identified by using a student questionnaire over the past year. Of 547 students with possible IgE-mediated food allergy, 243 (44.4%; 95% CI, 40.3% to 48.7%) reported a reaction to a food. Fifty-three (9.7%; 95% CI, 7.2% to 12.2%) students reported 93 anaphylaxis episodes. Peanut and tree nuts were the most common food triggers. Among students with current IgE-mediated food allergy, those with resolved or current asthma (adjusted odds ratio [aOR], 1.9 [95% CI, 1.1-1.3] and 1.7 [95% CI, 1.1-2.6]) and those with more than 2 food allergies (aOR, 1.9 [95% CI, 1.1-3.1]) were at greatest risk of any adverse food reaction, and those with nut allergy were most at risk of severe reactions (aOR, 2.9 [95% CI, 1.1-4.4]). Resolved or current asthma was not associated with increased risk of severe reactions (aOR, 0.8 [95% CI, 0.3-2.2] and 1.6 [95% CI, 0.7-3.7]). Adolescents with food allergy are frequently exposed to food allergens. Those with asthma and more than 2 food allergies were at the greatest risk for adverse food reactions. Those with nut allergies were most at risk of severe reactions.

Bifidobacteria의 allergy 면역 조절과 synergism

Allergy 질환은 지난 십여년 동안 개발도상국을 포함해서 전 세계적으로 증가하고 있다. Allergy 염증 반응은 수지상 세포와 같은 항원제시 세포에 의한 allergy 항원섭취를 시작으로 하여 Th2 면역 반응에 의해서 일어난다. 장내 미생물은 신체의 대사나 생리적 기능을 조절하고, 생애 초기의 면역 체계 성숙과 일생 동안 면역 체계 항상성 및 상피세포 총체성에 기여한다. Bifidobacteria는 Th1/Th2 balance에 strain-specific 한 면역 자극 특성을 가지며, TSLP와 IgE 발현을 억제 시키고 Flg과 FoxP3 발현을 촉진 시켜 allergy를 완화시킨다. 또한 Unmethylated CpG motif ODN은 B 세포와 수지상 세포의 TLR9에 의해 인식 되어 선천성과 적응성 면역 반응을 유도하고, Clostridium butyricum에 의해서 생산된 butyrate는 수지상 세포의 anti-inflammatory 유전자의 발현을 유도하기 위해 GPR109a signaling pathway를 활성화시키고, GPR43 활성화를 통하여 tTreg 세포 proliferation을 직접 자극하거나 HADC 활성을 억제시켜 Foxp3 gene intronic enhancer의 histone H3 acetylation을 통해 naive <TEX>$CD4^+$</TEX> T 세포를 pTreg 세포로 분화시킨다. Allergic diseases have increased over the past several decade worldwide including developing countries. Allergic inflammatory responses are caused by Th (T helper)2 immune responses, triggered by allergen ingestion by antigen presenting cells such as dendritic cells (DCs). Intestinal microorganisms control the metabolism and physiological functions of the host, contribute to early immune system maturation during the early life, and homeostasis and epithelial integrity during life. Bifidobacteria have strain-specific immunostimulatory properties in the Th1/Th2 balance, inhibit TSLP (thymic stromal lymphopoietin) and IgE expression, and promote Flg (Filaggrin) and FoxP3 (Treg) expression to alleviate allergies. In addition, unmethylated CpG motif ODN (oligodeoxynucleotides) is recognized by TLR (toll-like receptors)9 of B cells and plasmacytoid dendritic cells (pDCs) to induce innate and adaptive immune responses, while the butyrate produced by Clostridium butyricum activates the GPR (G-protein coupled receptors)109a signaling pathway to induce the expression of anti-inflammatory gene of pDCs, and directly stimulates the proliferation of thymically derived regulatory T (tTreg) cells through the activation of GPR43 or inhibits the activity of HADC (histone deacetylase) to differentiate naive <TEX>$CD4^+$</TEX> T cells into pTreg cells through the histone H3 acetylation of Foxp3 gene intronic enhancer.