Ingestion Of Allergen Research Articles

Timing of food introduction and atopy prevention

The apparent increase in atopic disease, particularly food allergy, over the past 2 decades has resulted in reconsideration of prevention strategies aimed at the infant’s diet. Early advice to have atopy-prone infants delay ingestion of potential food allergens, such as egg, cow’s milk, and peanut, was rescinded, as new evidence emerged that did not support these approaches. More recently, randomized controlled trials have provided data to support an opposite strategy, promoting early ingestion of allergens as a means of food allergy prevention. Specifically, new guidelines suggest early ingestion of peanut as a means to prevent peanut allergy. Additional dietary approaches regarding breastfeeding, early introduction of other types of food allergens, formula feeding, dietary nutrients, and probiotics are also under scrutiny as potential preventative strategies. This review focuses on the timing of food introduction as a preventative strategy for food allergy and also discusses other aspects of the infant diet that may provide opportunities for prevention of atopic disease.

Quality of life in childhood, adolescence and adult food allergy: Patient and parent perspectives.

Studies of children with food allergy typically only include the mother and have not investigated the relationship between the amount of allergen needed to elicit a clinical reaction (threshold) and health-related quality of life (HRQL). Our aims were (i) to compare self-reported and parent-reported HRQL in different age groups, (ii) to evaluate the impact of severity of allergic reaction and threshold on HRQL, and (iii) to investigate factors associated with patient-reported and parent-reported HRQL. Age-appropriate Food Allergy Quality of Life Questionnaires (FAQLQ) were completed by 73 children, 49 adolescents and 29 adults with peanut, hazelnut or egg allergy. Parents (197 mothers, 120 fathers) assessed their child's HRQL using the FAQLQ-Parent form. Clinical data and threshold values were obtained from a hospital database. Significant factors for HRQL were investigated using univariate and multivariate regression. Female patients reported greater impact of food allergy on HRQL than males did. Egg and hazelnut thresholds did not affect HRQL, but lower peanut threshold was associated with worse HRQL. Both parents scored their child's HRQL better than the child's own assessment, but whereas mother-reported HRQL was significantly affected by limitations in the child's social life, father-reported HRQL was affected by limitations in the family's social life. Severity of allergic reaction did not contribute significantly to HRQL. The risk of accidental allergen ingestion and limitations in social life are associated with worse HRQL. Fathers provide a unique perspective and should have a greater opportunity to contribute to food allergy research.

IL-9-producing cells in the development of IgE-mediated food allergy.

Food allergy is a harmful immune reaction driven by uncontrolled type 2 immune responses. Considerable evidence demonstrates the key roles of mast cells, IgE, and TH2 cytokines in mediating food allergy. However, this evidence provides limited insight into why only some, rather than all, food allergic individuals are prone to develop life-threatening anaphylaxis. Clinical observations suggest that patients sensitized to food through the skin early in life may later develop severe food allergies. Aberrant epidermal thymic stromal lymphopoietin and interleukin (IL) 33 production and genetic predisposition can initiate an allergic immune response mediated by dendritic cells and CD4+TH2 cells in inflamed skin. After allergic sensitization, intestinal IL-25 and food ingestion enhance concerted interactions between type 2 innate lymphoid cells (ILC2s) and CD4+TH2 cells, which perpetuate allergic reactions from the skin to the gut. IL-4 and cross-linking of antigen/IgE/FcεR complexes induce emigrated mast cell progenitors to develop into the multi-functional IL-9-producing mucosal mast cells, which produce prodigious amounts of IL-9 and mast cell mediators to drive intestinal mastocytosis in an autocrine loop. ILC2s and TH9 cells may also serve as alternative cellular sources of IL-9 to augment the amplification of intestinal mastocytosis, which is the key cellular checkpoint in developing systemic anaphylaxis. These findings provide a plausible view of how food allergy develops and progresses in a stepwise manner and that atopic signals, dietary allergen ingestion, and inflammatory cues are fundamental in promoting life-threatening anaphylaxis. This information will aid in improving diagnosis and developing more effective therapies for food allergy-triggered anaphylaxis.

The Emperor Has No Symptoms: The Risks of a Blanket Approach to Using Epinephrine Autoinjectors for All Allergic Reactions

Fatal anaphylaxis in humans is rare and unpredictable. We note a trend to provide allergic individuals with care plans that recommend immediate use of epinephrine autoinjectors if allergen ingestion is suspected, even in the absence of any allergic symptoms, without any supporting evidence base. Instructions to use an autoinjector device, irrespective of reaction severity and especially when symptoms are actually absent, are likely to add to parental and patient anxiety. Of greater concern is the possibility of epinephrine being administered “too early” to treat initial, mild symptoms that then progress to severe anaphylaxis. It is not hard to visualize a scenario where one or both epinephrine autoinjectors have been deployed for mild symptoms, yet the reaction progresses to a severe reaction and no further epinephrine is available for administration. Epinephrine needs to be available as a rescue treatment for anaphylaxis, potentially buying valuable minutes while emergency medical services are activated to attend. Food-allergic individuals and their carers need to be provided with more constructive strategies and support than merely being told to “use your pen.”

The Canadian Healthy Infant Longitudinal Development (CHILD) birth cohort study: assessment of environmental exposures.

The Canadian Healthy Infant Longitudinal Development birth cohort was designed to elucidate interactions between environment and genetics underlying development of asthma and allergy. Over 3600 pregnant mothers were recruited from the general population in four provinces with diverse environments. The child is followed to age 5 years, with prospective characterization of diverse exposures during this critical period. Key exposure domains include indoor and outdoor air pollutants, inhalation, ingestion and dermal uptake of chemicals, mold, dampness, biological allergens, pets and pests, housing structure, and living behavior, together with infections, nutrition, psychosocial environment, and medications. Assessments of early life exposures are focused on those linked to inflammatory responses driven by the acquired and innate immune systems. Mothers complete extensive environmental questionnaires including time-activity behavior at recruitment and when the child is 3, 6, 12, 24, 30, 36, 48, and 60 months old. House dust collected during a thorough home assessment at 3–4 months, and biological specimens obtained for multiple exposure-related measurements, are archived for analyses. Geo-locations of homes and daycares and land-use regression for estimating traffic-related air pollution complement time-activity-behavior data to provide comprehensive individual exposure profiles. Several analytical frameworks are proposed to address the many interacting exposure variables and potential issues of co-linearity in this complex data set.

Review: The role of antibodies, autoantigens and food allergens in canine atopic dermatitis.

Canine atopic dermatitis (AD) is considered to be an immunoglobulinE (IgE)-mediated hypersensitivity response to environmental allergens. The role of other antibody isotypes and nonenvironmental allergens in disease pathogenesis remains unclear. The objective of this review is to provide an update on advances in the understanding of the relevance of specific antibody isotypes, autoallergens and nonenvironmental allergens in the pathogenesis of canine AD. Citation databases, abstracts and proceedings from international meetings published between 2001 and 2013 were reviewed. Where necessary, older articles were included for background information. Neither total nor allergen-specific IgE necessarily correlates with clinical disease in canine AD. Some dogs exhibit clinical signs that are indistinguishable from AD but have no demonstrable allergen-specific IgE (atopic-like dermatitis). Allergen-specific immunoglobulinG may be demonstrated in canine AD, but there is no evidence that this isotype plays a role in disease development. Although humans with AD may develop serum IgE against autoallergens, this finding has not been substantiated in the dog. In contrast, adverse food reactions are frequently co-associated with AD in the dog. Ingestion of food and environmental allergens may trigger exacerbations of AD. Determination of the role of IgE in the pathogenesis of canine AD still requires clarification. Clinical trials and research studies must distinguish atopic dogs with allergen-specific IgE orskin test reactivity from those without. There is no convincing evidence demonstrating a pathogenic role for either allergen-specific immunoglobulinG or autoallergens in canine AD, but food items may be triggers for disease flares in certain individuals.

Immunoglobulin E Signal Inhibition during Allergen Ingestion Leads to Reversal of Established Food Allergy and Induction of Regulatory T Cells

Immunoglobulin E (IgE) antibodies are known for triggering immediate hypersensitivity reactions such as food anaphylaxis. In this study, we tested whether they might additionally function to amplify nascent antibody and T helper 2 (Th2) cell-mediated responses to ingested proteins and whether blocking IgE would modify sensitization. By using mice harboring a disinhibited form of the IL-4 receptor, we developed an adjuvant-free model of peanut allergy. Mast cells and IgE were required for induction of antibody and Th2-cell-mediated responses to peanut ingestion and they impaired regulatory T (Treg) cell induction. Mast-cell-targeted genetic deletion of the FcεRI signaling kinase Syk or Syk blockade also prevented peanut sensitization. In mice with established allergy, Syk blockade facilitated desensitization and induction of Treg cells, which suppressed allergy when transferred to naive recipients. Our study suggests a key role for IgE in driving Th2 cell and IgE responses while suppressing Treg cells in food allergy.

High resolution TaqMan real-time PCR approach to detect hazelnut DNA encoding for ITS rDNA in foods

A broad range of foods have been described as causing allergies, but the majority of allergic reactions can be ascribed to a limited number of food components. Recent extensive surveys showed how tree nuts, particularly hazelnut (Corylus avellana L.) seeds, rank amongst the most important sources of food allergy. In order to protect the allergic consumer, efficient and reliable methods are required for the detection of allergenic ingredients. For this purpose, we have developed a real-time polymerase chain reaction (PCR) for detection of hazelnut in commercial food products. In this way a specific hazelnut primer pair based on the ITS marker (70bp) and a nuclease (TaqMan) probe labelled with FAM and BHQ were designed. Sensibility of real-time PCR was determined by analysis of raw and heat treated hazelnut-wheat flour mixtures with a range of detection of 0.1–100,000ppm. Practical applicability of the real-time PCR assay developed for determining hazelnut in different food matrices was investigated by analyzing 179 commercial foodstuffs comprising snacks, biscuits, chocolates, bonbons, creams, nut bars, ice creams, precooked meals, breads, beverages, yogurts, cereals, meat products, rice cake and nougat. From the total of samples analyzed, 40 commercial food products that didn’t declare hazelnut nor traces on the label were found to contain hazelnut. The real-time PCR method proposed herein due to its high sensitivity facilitates the detection of hazelnut traces in commercial food products and can also be useful for monitoring the effectiveness of cleaning processes and as consequence, can help to prevent the food allergic consumer from unintentional ingestion of hidden allergens.

Sensitization to food allergens in Iranian children with mild to moderate persistent asthma

Asthma is the most common chronic respiratory disease in childhood. The clinical presentation of asthma may worsen after food allergen ingestion in sensitized patients. To avoid nonspecific dietary restrictions in children with asthma, laboratory-based advice about foods is potentially helpful. The purpose of this study was to determine food sensitization in children with asthma. Seventy-nine children with mild to moderate persistent asthma were included in this study. Commercial food allergens including cow's milk, egg white, almond, potato, and soybean were used in skin prick tests. Specific IgE to 20 common food allergens was also measured in serum. Twelve (15.2%) of the patients had a positive skin prick test to at least one of the five food extracts. Sensitization was detected by skin prick tests to cow's milk and egg white (each 6.3%), almond (3.8%), potato (2.5%) and soybean (1.3%). Specific IgE levels ≥0.35 kAU/L were detected in the serum of 47% of the children with asthma. The most common food allergens were cow's milk (26.6%), hazelnuts (25.3%), wheat flour (15.2%) and egg white (12.6%). Patients with a history of at least one hospital admission due to asthma attack had a higher rate of sensitization to egg. In our study, food sensitization was frequent in Iranian children with asthma. Although clinical food allergy could not be evaluated because food challenge tests were not used in our study, skin prick tests and serum-specific IgE to common food allergens might be helpful in identifying children with food sensitization.

Alergia às proteínas do leite de vaca em adolescente com anafilaxia: uma opção terapêutica inovadora

Cow's milk allergy (CMA) is an increasingly prevalent disease, with longer duration. The elimination diet is often difficult and so adverse reactions by ingestion of hidden allergen are common. We report the case of an adolescent with a history of severe CMA, with several episodes of anaphylaxis after accidental ingestion of cow's milk (CM), successfully submitted to a CM tolerance induction protocol, reaching a daily dose of 200 ml, which allowed a free diet. Applied by experienced staff in specialized medical centers, this seems to be an innovative therapeutic strategy also in severe cases of CMA, modifying its natural history and conferring protection against hidden allergen ingestion, allowing a significant improvement in quality of life. Its disclosure is important so that the best treatment options are offered to these patients.

A prediction rule for food challenge outcome in children

In children with food-related symptoms, a food challenge is considered as the gold standard to diagnose allergy. If food allergy could be predicted by patient history and/or diagnostic tests, the number of time-consuming and sometimes risky food challenges could be decreased. We aimed to determine questionnaire and test-based characteristics, to predict the food challenge outcome (FCO) in children referred to a tertiary centre for the evaluation of food-related symptoms. Pre-challenge standardized questionnaires, skin prick tests (SPT), and specific IgE levels (sIgE) were obtained in patients that underwent a food challenge in our hospital in 2009. Characteristics of patients with positive and negative FCO were compared, and uni- and multivariate associations between predictors and FCO were calculated. Based on the multivariate model, a risk score was developed to predict the FCO. One hundred and twenty-nine challenges were analyzed, 41.9% had a positive outcome. Median age of both groups was 4.9 yrs (range 2.8-8.3). Patients with a positive FCO reacted faster with symptoms after allergen ingestion and had higher sIgE levels compared to children with negative FCO. A clinical risk score was developed based on the index food, 'time between allergen ingestion and complaints' and sIgE levels (range 0-10). The prognostic capacity of this model (AUC) was excellent (0.90). The very high- and low-risk groups (24% of patients) are both predicted excellent without misclassification. Positive FCO can be predicted by the index food, time between allergen ingestion and development of symptoms, and the sIgE level.

Anaphylaxis associated with exercise

Exercise-induced Anaphylaxis (EIA) is a rare, unpredictable, potentially fatal, syndrome characterised by anaphylaxis associated with exercise. Anaphylaxis is associated with a mortality rate of between 1-2%; importantly, some 5-15% of anaphylactic episodes are caused by /or are associated with exercise. EIA may occur independently of food allergen ingestion, or may require the ingestion of a food allergen around the time of exercise, known as Food-dependent exercise-induced anaphylaxis (FDEIA). Concomitant medication use may also be required as an additional facilitating factor, known as ‘summation anaphylaxis'. There are now more than one hundred reviews on the topic of EIA (food dependent and non-food dependent) upon which much of our current knowledge of the condition is based. The aim of this presentation is to draw on key clinical features of these conditions; we will then either support, or challenge, existing hypotheses with respect to exercise-induced pathophysiological mechanisms that may underlie EIA. This will be in the context of recent advances in our understanding of exercise physiology.

Labeling of ethnic food in the Prato Chinese community

Ethnic food consumption is a quickly growing reality within Chinese communities, which have a well-organized "internal" food market for both Asian and ethnic foods produced in the European Union. The main problems associated with these markets are related to hygienic conditions, certifications of accomplishment, and personnel management. Moreover, controls and identification of the products are difficult because of cultural and linguistic barriers. In this study, five markets managed by the Chinese were visited, and the conformity of the reported label information found on different kinds of food (prepackaged or loose) was assessed by a collaboration between the Local Authorities of Control of the Prato territory, which hosts the largest Chinese community in Italy, and of native speakers of Chinese. All visited markets presented products (n = 75) with non-conformities: lack of translation (6%) and incomplete/mistaken translation of the commercial name (72%) and place of production (12%). In addition to the legal implications of the observed non-compliances, certain sanitary issues were taken into consideration. In fact, a number of the products that belong to risk categories could be misclassified in a non-risk category. Lastly, missing ingredients or complete alteration of their commercial names may represent health threats in cases of allergen ingestion by allergic or intolerant consumers.

Clinical laboratory assessment of immediate-type hypersensitivity

Clinical laboratory analyses aid in the diagnosis and management of human allergic (IgE-dependent) diseases. Diagnosis of immediate-type hypersensitivity begins with a thorough clinical history and physical examination. Once symptoms compatible with an allergic disorder have been identified, a skin test, blood test, or both for allergen-specific IgE antibodies provide confirmation of sensitization, which strengthens the diagnosis. Skin testing provides a biologically relevant immediate-type hypersensitivity response with resultant wheal-and-flare reactions within 15 minutes of allergen application. Allergen-specific IgE antibody in serum is quantified by using 3 laboratory-based autoanalyzers (ImmunoCAP, Immulite, and HYTEC-288) and novel microarray and lateral-flow immunoassays. Technologic advances in serologic allergen-specific IgE measurements have involved increased automation, with enhanced reproducibility, greater quantification, lower analytic sensitivity, and component-supplemented extract-based allergen use. In vivo provocation tests involving inhalation, ingestion, or injection of allergens serve to clarify discordant history and skin- or blood-based measures of sensitization. Other diagnostic allergy laboratory analyses include total and free serum IgE measurement, precipitating IgG antibodies specific for organic dusts, mast cell tryptase, and indicator allergen analyses to assess indoor environments to promote patient-targeted allergen avoidance programs. A critique is provided on the predictive utility of serologic measures of specific IgE for food allergy and asthma. Reasons for the lack of clinical utility for food-specific IgG/IgG4 measurements in allergy diagnosis are examined. When the specific IgE measures are inconsistent with the clinical history, they should be confirmed by means of repeat and alternative method analysis. Ultimately, the patient's clinical history remains the principal arbiter that determines the final diagnosis of allergic disease.

Epicutaneous antigen challenge of orally sensitized mice elicits allergic dermatitis by redirecting α4β7 gut homing T cells to the skin (79.7)

Abstract Patients with atopic dermatitis (AD) can develop skin flares after ingestion of food allergens or cutaneous contact with these antigens. We examined the mechanism by which cutaneous exposure to allergens in orally sensitized individuals may elicit allergic skin inflammation. Wild-type (WT) or CC chemokine receptor (CCR)4-/- mice were fed intragastrically once a week for eight weeks 5 mg ovalbumin (OVA) and 10 μg cholera toxin (CT) in 200 μL saline or with CT alone in saline. Mice were then epicutaneously (EC) challenged with 100 μg OVA or saline. Mice were sacrificed a week later and analyzed for allergic skin inflammation. For adoptive transfer, CD4+α4β7+ T cells were purified from mesenteric lymph node (MLN) of orally sensitized WT or CCR4-/- mice and administered to WT recipients followed by EC challenge with OVA. Mice orally immunized with OVA then EC challenged with OVA developed allergic skin inflammation characterized by dermal infiltration with eosinophils and CD4+ T cells and upregulation of Th2 cytokines mRNA expression. In contrast to WT mice, orally immunized CCR4-/- mice failed to develop allergic skin inflammation in response to EC challenge. Purified CD4+α4β7+ T cells from MLN of orally immunized WT mice, but not CCR4-/- mice, transferred allergic skin inflammation to WT recipients. These results suggest that CD4+α4β7+ T cells educated in the gut can be reprogrammed in vivo to home to the skin in a CCR4 dependent manner and cause allergic skin inflammation in response to cutaneous antigen exposure. Funded by The Atopic Dermatitis and Vaccinia Network NIH/NIAID contract N01 AI40030

Breathing easier with breast milk

Breast milk protects young mice from developing symptoms of asthma. The effect occurs through the induction of regulatory T cells after ingestion of allergen and TGF-β in breast milk (pages 170–175).

Studies on the role of routes of allergen exposure in high IgE‐producing beagle dogs sensitized to house dust mites

The current study aimed to investigate the role played by oral, epicutaneous, and inhalation routes of exposure to house dust mites (HDM). The colony of high IgE-producing beagle dogs has been shown to develop pruritic dermatitis compatible with atopic dermatitis following environmental exposure (EE) to HDM. In crossover experiments, the response to EE was compared to two modified challenges, oral exposure (OE) and snood and muzzle exposure (SME). For OE, HDM were fed daily for 3 days. For SME, ingestion of allergen was prevented but there was inhalation and epicutaneous exposure to all body regions except to one ear. In all experiments, dogs were challenged for three consecutive days, and evaluated before, 6 h after exposure and daily thereafter, for 5 days. After a wash-out period, groups were crossed-over so that each dog was randomly challenged to all three protocols. Clinical scores were analysed using least squares analysis of variance. All dogs developed pruritic dermatitis regardless of the protocol. With OE, lesions developed in the same body regions as with EE although scores were lower. This difference became more evident after the first 3 days when OE scores decreased and EE scores continued to increase. The scores of covered and uncovered ears did not differ with SME. Scores for the remainder of the body were significantly lower than for EE. The development of lesions on covered ears supports the importance of inhalation or a systemic reaction to epicutaneous exposure in other areas. It is concluded that all routes are important and have additive effects, that route of exposure does not determine the distribution of lesions and that continuous epicutaneous exposure probably plays the most important role.

Response of Respiratory Flour Allergics in an Ingested Flour Challenge May Involve Plasmacytoid Dendritic Cells, CD25+ and CD152+ T Cells

Background: A number of occupational respiratory allergens are food related, and little is known about the responses these allergens elicit in sensitized persons that ingest them. Methods: Nine respiratory flour-allergic volunteers were exposed in a double-blind placebo-controlled food challenge with flour. Responses were monitored by spirometry, acoustic rhinometry, determination of urinary methyl histamine and tryptase and flow cytometric evaluation of basophil, dendritic and T cell numbers and markers. Results: Significant increases in serum tryptase (compared with placebo post-exposure levels) and methyl histamine and a coordinated decrease in blood basophils and nasal volume after ingestion of allergen compared with placebo suggest an allergic response to ingested allergen. There was no change in forced expiratory volume in 1 s. The number of blood plasmacytoid dendritic cells (DC), but not of myeloid DC, decreased after exposure (p = 0.001). DC HLA DR was reduced after both exposures (p < 0.001). Expression of CXCR4 on DC was reduced after allergen (p = 0.033) but not after placebo exposure. CD4+ T cell expression of CD25 was elevated after placebo (p = 0.021) but reduced after allergen provocation. The reduction in CD25 expression after allergen compared with placebo was significant (p = 0.024). CD152 was downregulated on these cells after allergen (p = 0.039) but less so after placebo exposure. Conclusion: Persons with respiratory allergy respond after ingestion of the relevant allergen. Response to this allergen challenge may selectively recruit plasmacytoid DC through CXCR4 and T cells expressing CD25 and CD152, which may be a regulatory phenotype.

Asthma: A Gut Reaction to Antibiotics

Is the explosive rise in asthma and allergies being seen especially in children partially related to antibiotic use? Epidemiologic studies have found strong connections between antibiotic treatment and the later development of asthma and allergies. Yet, until recently, no studies had looked at how the two are linked. Now researchers at the University of Michigan in Ann Arbor have created a mouse model that offers clues to the mechanism behind the association. Immunologist Gary Huffnagle and colleagues are the first to demonstrate in a mouse model that the disruption of beneficial intestinal bacteria by antibiotics allows yeast to take hold and flourish. They developed their mouse model specifically to study the relationship between antibiotic use and allergies. When mice inhale fungal spores known to trigger allergies in people, the allergic reaction is more potent in mice with an overgrowth of yeast in their guts. In their studies, the Michigan researchers first treat mice for several days with the broad-spectrum antibiotic cefoperazone to destroy the gut flora. Then the mice are fed Candida albicans, a yeast that commonly lives in people. “This represents the clinical scenario of getting a yeast infection after taking antibiotics,” says Huffnagle. Next, the mice are exposed nasally to spores of the mold Aspergillus fumigatus (a major indoor contaminant) and to egg white protein. Results are showing that both allergens produce significant increases in inflammation-related white blood cells in the lungs of the mice, and they elevate blood levels of key markers of allergic reactions, including IgE, interleukin-5, and interleukin-13. Mice not treated with antibiotics show much milder reactions to the allergens. The team’s latest report appears in the January 2005 issue of Infection and Immunity. Future work with the model will investigate the actions of other antibiotics (such as amoxicillin) and allergens (such as pollen and dust mites). How do changes in gut flora influence respiratory allergies? The answer likely involves oral tolerance, Huffnagle theorizes. Upon ingestion of allergens, the oral mucosa generate regulatory T cells, which circulate to the respiratory tract, where they suppress allergic reactions. “We live in a dirty world, and we swallow mold spores, pollen, dust, and other allergens constantly,” says Huffnagle. These oral allergens trigger immune responses that instruct the rest of the body to be more tolerant of allergens so allergic reactions don’t occur. Moreover, other studies have indicated that mice lacking gut flora cannot generate oral tolerance. When the gut flora are restored, oral tolerance returns. Huffnagle plans to evaluate over-the-counter probiotics—concentrated supplements of beneficial bacteria—to identify which, if any, work best for replenishing gut flora. “[Probiotics are a] relatively new concept, and there’s not a lot of precedent for their use now,” says infectious disease specialist Bruce Klein of the University of Wisconsin–Madison. If future studies show that probiotics do replace flora, Klein adds, physicians may be inclined to recommend their use. Eating yogurt with live cultures also remains a good way to replenish gut flora following a course of antibiotics.

Intestinal IgE secretion in food allergy: Potential role for CD23 isoforms on intestinal epithelial cells

Rationale Anaphylactic reactions can occur extremely rapidly after ingestion of food allergens. A CD23/IgE-dependent antigen uptake mechanism is required for rapid hypersensitivity reactions in rodent models of food allergy. The mechanism leading to lumenal IgE remains unknown. Methods Naïve and sensitized (OVA and casein) C3H/HeJ mice were used. Specific IgE was measured in intestinal lavage from mice, and in stool samples from food allergic patients. Intestinal secretion of IgE and IgG were compared by injection of mice with 125I-IgE or -IgG and measurement of 125I in intestinal lavage and stool. CD23 expression was determined by immunohistochemistry and RT-PCR. IgE uptake by intestinal epithelial cells (IEC) was determined by confocal microscopy. Results Allergen-specific IgE was detected in stool samples from food-allergic patients, and in intestinal lavage fluid from sensitized mice. Sensitized mice secreted greater levels of 125I-IgE, and to a lesser extent 125I-IgG, into the intestinal lumen compared to naïve mice. Sensitization was associated with upregulated CD23 expression on mouse IEC. RT-PCR analysis of CD23 isoform expression in IEC obtained from patients with food allergic disorders or normal controls demonstrated that the CD23a isoform was constitutively expressed, while the CD23b isoform was present only in IEC from food allergic patients. Polarized caco-2 cells transfected with the CD23a isoform rapidly internalized FITC-IgE from the apical, but not the basolateral domain. Conclusions Allergen-specific IgE is secreted into the intestinal lumen in sensitized individuals, and may facilitate uptake of antigen by interaction with CD23a. Upregulation of the CD23b isoform may be responsible for the secretion of IgE into the intestinal lumen.