B cells are involved in the modulation of pathogenic gut immune response in food-allergic enteropathy

Cardoso, Cristina Ribeiro de Barros; Provinciatto, Pauline R.; Godoi, Dannielle Fernandes; Vieira, Thalita Silva; Ferreira, Beatriz Rossetti; Teixeira, Gerlinde Agate Platais Brasil; Rossi, Marcos A.; Cunha, Fernando; Silva, João

doi:10.1111/j.1365-2249.2008.03748.x

Cited by 9 publications

(8 citation statements)

References 38 publications

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“…Similar results were obtained by others in BALB/c mice orally sensitized with CMP or peanut [34]. In the same sense, Cardoso et al [3], in a food allergy mouse model developed in C57BL/6 mice, showed that skin sensitization with peanut and alum induced a gut-inflammatory response after feeding mice with peanuts. Although they found a significant induction of IL-4 and IL-13, no increase in IL-5 and IFN-γ was detected.…”

Section: Discussionsupporting

confidence: 72%

“…These models have unveiled different aspects of mucosal immunity that occur after the breakdown of oral tolerance to ingested nutrients [1,2]. They have evolved from systemic to mucosal sensitization protocols with the consequent induction of anaphylaxis-like IgE-mediated reactions that mimics the human disease upon allergen challenge [3,4,5]. Due to the immune tolerance to antigens encountered in the gastrointestinal mucosa [6], adjuvants are commonly used to abrogate this complex and not fully understood process [7].…”

Section: Introductionmentioning

confidence: 99%

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In vivo Evidence of Cross-Reactivity between Cow’s Milk and Soybean Proteins in a Mouse Model of Food Allergy

Smaldini¹,

Curciarello²,

Candreva³

et al. 2012

Int Arch Allergy Immunol

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Background: Cow’s milk allergy (CMA) is an important problem worldwide and the development of an in vivo system to study new immunotherapeutic strategies is of interest. Intolerance to soybean formula has been described in CMA patients, but it is not fully understood. In this work, we used a food allergy model in BALB/c mice to study the cross-reactivity between cow’s milk protein (CMP) and soy proteins (SP). Methods: Mice were orally sensitized with cholera toxin and CMP, and then challenged with CMP or SP to induce allergy. Elicited symptoms, plasma histamine, humoral and cellular immune response were analyzed. Th1- and Th2-associated cytokines and transcription factors were assessed at mucosal sites and in splenocytes. Cutaneous tests were also performed. Results: We found that the immediate symptoms elicited in CMP-sensitized mice orally challenged with SP were consistent with a plasma histamine increase. The serum levels of CMP-specific IgE and IgG1 antibodies were increased. These antibodies also recognized soy proteins. Splenocytes and mesenteric lymph node cells incubated with CMP or SP secreted IL-5 and IL-13. mRNA expression of Th2-associated genes (IL-5, IL-13, and GATA-3) was upregulated in mucosal samples. In addition, sensitized animals exhibited positive cutaneous tests after the injection of CMP or SP. Conclusions: We demonstrate that CMP-sensitized mice, without previous exposure to soy proteins, elicited hypersensitivity signs immediately after the oral administration of SP, suggesting that the immunochemical cross-reactivity might be clinically relevant. This model may provide an approach to further characterize cross-allergenicity phenomena and develop new immunotherapeutic treatments for allergic patients.

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Section: Discussionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

In vivo Evidence of Cross-Reactivity between Cow’s Milk and Soybean Proteins in a Mouse Model of Food Allergy

Smaldini¹,

Curciarello²,

Candreva³

et al. 2012

Int Arch Allergy Immunol

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“…), one patient with c.667G>T and one patient with c. 1384G>T [72] have somatic mosaicisms of cells with the mutated CYBB sequence and a small proportion of reverse mutated cells with the wild-type CYBB sequence. …”

Section: Tablementioning

confidence: 99%

Hematologically important mutations: X-linked chronic granulomatous disease (third update)

Roos

Kuhns

Maddalena³

et al. 2010

Blood Cells, Molecules, and Diseases

188

175

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Chronic Granulomatous Disease (CGD) is an immunodeficiency disorder affecting about 1 in 250,000 individuals. The disease is caused by a lack of superoxide production by the leukocyte enzyme NADPH oxidase. Superoxide is used to kill phagocytosed micro-organisms in neutrophils, eosinophils, monocytes and macrophages. The leukocyte NADPH oxidase is composed of five subunits, of which the enzymatic component is gp91-phox, also called Nox2. This protein is encoded by the CYBB gene on the × chromosome. Mutations in this gene are found in about 70% of all CGD patients. This article lists all mutations identified in CYBB in the X-linked form of CGD. Moreover, apparently benign polymorphisms in CYBB are also given, which should facilitate the recognition of future disease-causing mutations.

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“…To test this hypothesis, follicular B cells should be isolated and activated with or without bortezomib treatment, and then analyzed in more detail with respect to proliferation and isotype switching ex vivo. Furthermore, previous data indicated that B-cell-deficient mice have less allergen-induced diarrhea than wild-type mice, followed by less plasma cell accumulation in the intestine [33,34]. Interestingly, blocking of CD23 with anti-CD23 completely abolished the antigen uptake in sensitized mice.…”

Section: Discussionmentioning

confidence: 89%

Bortezomib treatment diminishes hazelnut‐induced intestinal anaphylaxis in mice

et al. 2016

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Food allergy is a common health problem and can cause anaphylaxis. Avoidance of the offending food allergen is still the mainstay therapeutic approach. In this study, we investigated the role of plasma cell reduction by proteasome inhibition in a murine model of food allergy and examined the impact of this treatment on the systemic and local immune response. For this purpose, intestinal anaphylaxis was induced in BALB/c mice with the food allergen hazelnut, in conjunction with different adjuvants (alum and Staphylococcal enterotoxin B SEB) and different administration routes (oral and intraperitoneal). In both models, allergy symptoms were observed, but the clinical severity was more pronounced in the hazelnut-alum model than in the hazelnut-SEB model. Accordingly, allergen-specific immunoglobulin E (IgE) against hazelnut was detectable, and mast cell protease-1 in serum was increased after allergen provocation. Treatment with the proteasome inhibitor bortezomib reduced plasma cells and resulted in an abolishment of hazelnut allergen-specific IgE, which was associated with amelioration of clinical symptoms as well as a significant decrease in both CD19 + and follicular B lymphocytes. Our data demonstrate the importance of allergen-specific IgE in food allergy and point to B cells as potential therapeutic targets for its treatment. Keywords: Anaphylaxis B cells Food allergy Immunoglobulin E Proteasome inhibitionAdditional supporting information may be found in the online version of this article at the publisher's web-site IntroductionAllergic reactions to food are common, and in most cases are caused by type 1-mediated hypersensitivity reactions [1]. Severe cases of food allergy may result in anaphylaxis, which can be fatal [1,2]. Features of food allergy include sensitization paramCorrespondence: Univ. Prof. Dr. med. Margitta Worm e-mail: margitta.worm@charite.de eters, such as the presence of allergen-specific immunoglobulin E (IgE), and typical clinical symptoms. These frequently consist of skin symptoms, such as urticaria and/or angioedema, but also include variable systemic responses, such as respiratory and cardiovascular symptoms [1][2][3]. Until now, the primary therapeutic approach for patients with food allergy has been strict avoidance of the offending food allergen [1]. Hazelnut (Corylus avellana) is a common cause of food allergy in Europe [4][5][6][7], and affects 0.1-0.5% of the population [8]. Hazelnut-allergic Eur. J. Immunol. 2016. 46: 1727-1736 a risk of severe or even fatal reactions [4][5][6]. Although sublingual immunotherapy and/or oral tolerance-induction has recently been shown to be effective for the treatment of peanut-allergic patients [9,10], their use in clinical practice is limited and currently restricted to specialized centers because of the risk of severe side effects. Another therapeutic approach to treat food allergy is the depletion of IgE. Indeed, the efficacy of an anti-IgE treatment has been demonstrated in patients suffering from food allergy [11]. Likewise, the anti-Ig...

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B cells are involved in the modulation of pathogenic gut immune response in food-allergic enteropathy

Abstract: Summary Food enteropathies involve uncontrolled or hypersensitivity reactions to ingested nutrients and may result in

Cited by 9 publications

References 38 publications

In vivo Evidence of Cross-Reactivity between Cow’s Milk and Soybean Proteins in a Mouse Model of Food Allergy

In vivo Evidence of Cross-Reactivity between Cow’s Milk and Soybean Proteins in a Mouse Model of Food Allergy

Hematologically important mutations: X-linked chronic granulomatous disease (third update)

Bortezomib treatment diminishes hazelnut‐induced intestinal anaphylaxis in mice

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