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      Is Open Access

      Elimination diet in food allergy: friend or foe?

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          Abstract

          Abstract Objectives To review and discuss the role of an elimination diet in food-allergic children, emphasizing nutritional aspects for a better practical approach. Sources Non-systematic review of the literature. Findings Under an elimination diet, food-allergic patients may suffer from growth impairment or obesity and compromised quality of life. Disease phenotype, age, type, number of foods excluded, comorbidities, eating difficulties, economic status, and food availability must be considered for an appropriate diet prescription. Diet quality encompasses diversity and degree of food processing, which may alter immune regulation. Conclusions A friendly food elimination diet prescription depends on a multidisciplinary approach beyond macro and micronutrients.

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          Most cited references67

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          Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells.

          Gut commensal microbes shape the mucosal immune system by regulating the differentiation and expansion of several types of T cell. Clostridia, a dominant class of commensal microbe, can induce colonic regulatory T (Treg) cells, which have a central role in the suppression of inflammatory and allergic responses. However, the molecular mechanisms by which commensal microbes induce colonic Treg cells have been unclear. Here we show that a large bowel microbial fermentation product, butyrate, induces the differentiation of colonic Treg cells in mice. A comparative NMR-based metabolome analysis suggests that the luminal concentrations of short-chain fatty acids positively correlates with the number of Treg cells in the colon. Among short-chain fatty acids, butyrate induced the differentiation of Treg cells in vitro and in vivo, and ameliorated the development of colitis induced by adoptive transfer of CD4(+) CD45RB(hi) T cells in Rag1(-/-) mice. Treatment of naive T cells under the Treg-cell-polarizing conditions with butyrate enhanced histone H3 acetylation in the promoter and conserved non-coding sequence regions of the Foxp3 locus, suggesting a possible mechanism for how microbial-derived butyrate regulates the differentiation of Treg cells. Our findings provide new insight into the mechanisms by which host-microbe interactions establish immunological homeostasis in the gut.
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            Interleukins (from IL-1 to IL-38), interferons, transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases

            There have been extensive developments on cellular and molecular mechanisms of immune regulation in allergy, asthma, autoimmune diseases, tumor development, organ transplantation, and chronic infections during the last few years. Better understanding the functions, reciprocal regulation, and counterbalance of subsets of immune and inflammatory cells that interact through interleukins, interferons, TNF-α, and TGF-β offer opportunities for immune interventions and novel treatment modalities in the era of development of biological immune response modifiers particularly targeting these molecules or their receptors. More than 60 cytokines have been designated as interleukins since the initial discoveries of monocyte and lymphocyte interleukins (called IL-1 and IL-2, respectively). Studies of transgenic or gene-deficient mice with altered expression of these cytokines or their receptors and analyses of mutations and polymorphisms in human genes that encode these products have provided essential information about their functions. Here we review recent developments on IL-1 to IL-38, TNF-α, TGF-β, and interferons. We highlight recent advances during the last few years in this area and extensively discuss their cellular sources, targets, receptors, signaling pathways, and roles in immune regulation in patients with allergy and asthma and other inflammatory diseases.
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              Advanced glycation end products in foods and a practical guide to their reduction in the diet.

              Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake. 2010 American Dietetic Association. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                jped
                Jornal de Pediatria
                J. Pediatr. (Rio J.)
                Sociedade Brasileira de Pediatria (Porto Alegre, RS, Brazil )
                0021-7557
                1678-4782
                April 2024
                : 100
                : suppl 1
                : S65-S73
                Affiliations
                [2] Santo André SP orgnameCentro Universitário Faculdade de Medicina do ABC orgdiv2Departamento de Pediatria Brazil
                [1] São Paulo orgnameUniversidade Federal de São Paulo orgdiv1Departamento de Pediatria orgdiv2Divisão de Alergia, Imunologia Clínica e Reumatologia Brazil
                Article
                S0021-75572024000700108 S0021-7557(24)10000000108
                10.1016/j.jped.2023.09.012
                708798f1-32b9-4759-95a2-24b92682e626

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 20 September 2023
                : 17 September 2023
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 60, Pages: 0
                Product

                SciELO Brazil

                Categories
                Review Article

                Advanced glycation end products,Food hypersensitivity,Children,Adolescents,Dietary intake,Immune system

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