Quantitative Analysis and Immunohistochemical Studies on Small Intestinal Mucosa of Food-Sensitive Enteropathy

Nagata, Satoru; Yamashiro, Yuichiro; Ohtsuka, Yoshikazu; Shioya, T.; Oguchi, Satoshi; Shimizu, Tomoharu; Maeda, Masato

doi:10.1097/00005176-199501000-00008

Cited by 37 publications

(18 citation statements)

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“…↑ IFN-γ and IL-4 in jejunal biopsy [80] Cellular changes ↑ Eosinophils in intestinal biopsies, blood, and stool [35,73] ↑ CD4+ T cells and plasma cells from biopsy [81] From colonic biopsies:…”

Section: Managementmentioning

confidence: 99%

Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy

Feuille

Nowak‐Węgrzyn

2015

Curr Allergy Asthma Rep

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Food protein-induced enterocolitis (FPIES), allergic proctocolitis (FPIAP), and enteropathy (FPE) are among a number of immune-mediated reactions to food that are thought to occur primarily via non-IgE-mediated pathways. All three are typically present in infancy and are triggered most commonly by cow's milk protein. The usual presenting features are vomiting with lethargy and dehydration in FPIES; bloody and mucous stools in FPIAP; and diarrhea with malabsorption and failure to thrive in FPE. Diagnosis is based on convincing history and resolution of symptoms with food avoidance; confirmatory diagnostic testing other than food challenge is lacking. The mainstay of management is avoidance of the suspected inciting food, with interval challenge to assess for resolution, which usually occurs in the first years of life. Studies published in the past few years clarify common presenting features, report additional culprit foods, address potential biomarkers, and suggest new management strategies.

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Section: Managementmentioning

confidence: 99%

Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy

Feuille

Nowak‐Węgrzyn

2015

Curr Allergy Asthma Rep

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“…Milk exposure leads to increased intraepithelial lymphocytes, including an increase in those expressing the TIA1, a marker of cytotoxic granules 24 . There is also an increase in CD4+ T cells in the lamina propria bearing the activation marker HLA-DR 25 . Plasma cells producing IgM and IgA are increased in number during milk exposure, as are eosinophils 11, 12 .…”

Section: Introductionmentioning

confidence: 99%

Immunopathophysiology of food protein–induced enterocolitis syndrome

Berin

2015

Journal of Allergy and Clinical Immunology

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There is increasing recognition of the non-IgE-mediated gastrointestinal food allergy known as food protein-induced enterocolitis syndrome (FPIES), with several recent publications summarizing the clinical experience with FPIES in the US, the UK, Europe, and Australia. Our understanding of the mechanisms linking food exposure to typical symptoms of vomiting, hypotension, and diarrhea has lagged far behind our understanding of the immune mechanisms of IgE-mediated food allergy. The goal of this overview is to summarize and critique the current state of knowledge of the immunology of FPIES, and to identify major gaps in our knowledge that need to be addressed in order to make significant gains in developing therapies and prevention strategies for FPIES.

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“…Type I or IgEmediated allergic reactions are involved in early-phase symptoms of food allergy (6,8). On the other hand, cell-mediated reactions are also involved in the late phase and symptoms are often prolonged, causing mucosal damage such as crypt hyperplasia, villus atrophy, and lymphocyte infiltration (11,13,27,30). Because human research is restricted, animal models of food allergies would be of significant value.…”

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confidence: 99%

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

Ogawa

Miura²,

Tsuzuki³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1. Am J Physiol Gastrointest Liver Physiol 286: G702-G710, 2004. First published December 11, 2003 10.1152/ajpgi.00183.2003.-Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.Brown Norway rats; rat mast cell protease II; delayed type hypersensitivity; Peyer's patch; intercellular adhesion molecule-1 THE CLINICAL MANIFESTATIONS of allergic reactions from food intolerance may be localized to the gut, including abdominal discomfort, nausea, vomiting, and diarrhea. Type I or IgEmediated allergic reactions are involved in early-phase symptoms of food allergy (6,8). On the other hand, cell-mediated reactions are also involved in the late phase and symptoms are often prolonged, causing mucosal damage such as crypt hyperplasia, villus atrophy, and lymphocyte infiltration (11,13,27,30). Because human research is restricted, animal models of food allergies would be of significant value. Several efforts have been made to develop rodent models of food allergy (10,14,32). However, few models have been validated for studying the effects of chronic antigen exposure or for relevance to clinical situations involving both IgE-and cell-mediated reactions (21,22,28). Although several groups (10) have investigated the effect of repeated oral challenge in rats with IgEmediated hypersensitivity, lymphocyte infiltration was not obvious in the intestinal mucosa of these animals. Only a recent report by Yang et al. (36) has demonstrated that the oral antigen challenge of sensitized Sprague-Dawley rats induces sustained epithelial dysfunction with inflammator...

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Quantitative Analysis and Immunohistochemical Studies on Small Intestinal Mucosa of Food-Sensitive Enteropathy

Cited by 37 publications

References 0 publications

Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy

Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy

Immunopathophysiology of food protein–induced enterocolitis syndrome

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

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