IgE-Positive Cells in Human Intestinal Mucosa Are Mainly Mast Cells

Rognum, Torleiv O.; Brandtzæg, Per

doi:10.1159/000234956

Cited by 27 publications

(8 citation statements)

References 28 publications

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“…There is an increase in the number of IgE‐bearing mast cells in the intestinal mucosa and submucosa of food allergic patients and in mouse models (Fig. ) .…”

Section: Mechanisms Of Food Intolerancementioning

confidence: 97%

Food intolerance and mucosal inflammation

Ohtsuka

2015

Pediatrics International

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Most infants are immunologically active and are able to develop a tolerance to oligoclonal antigens by producing IgA, along with activation of regulatory T cells, in early infancy. Cytokines and their signaling molecules are important mediators in the intestine, regulating both oral tolerance and mucosal inflammation. This system works efficiently in most individuals, but for an as yet undefined reason, some people react to food and other proteins as though they were pathogens, with induction of chronic inflammation in the mucosa. The adverse reaction caused by ingested foods is defined as food intolerance. The clinical features of food intolerance include vomiting, diarrhea, bloody stool, eczema, failure to thrive, and a protean range of other symptoms. Intolerance can be divided into two categories depending on whether or not they are immunologically mediated. Food intolerance and mucosal inflammation are deeply related because tolerance cannot be established when there is an inflammation in the intestinal mucosa. Mast cells, eosinophils, mucosal lymphocytes, and epithelial cells are deeply involved and related to each other in the development of mucosal inflammation. Meanwhile, rectal bleeding in infancy is related to lymphoid hyperplasia with eosinophil infiltration into the colonic mucosa facilitated by C-C motif ligand 11 (CCL11, known as eotaxin-1) and C-X-C motif chemokine ligand 13 (CXCL13). Rectal bleeding in infancy may not be simply caused by allergic reactions against specific antigens, but may be due to migrated lymphocytes developing immunological tolerance; including IgA synthesizing, in the intestinal mucosa.

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“…There is an increase in the number of IgE‐bearing mast cells in the intestinal mucosa and submucosa of food allergic patients and in mouse models (Fig. ) .…”

Section: Mechanisms Of Food Intolerancementioning

confidence: 97%

Food intolerance and mucosal inflammation

Ohtsuka

2015

Pediatrics International

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“…The tissue specimens were immediately fixed in cold ethanol before being processed for paraffin embed ding [9]. Serial sections were cut at 6 um and incubated with a mu rine monoclonal antibody to human IgE (Serotec, Kidlington, Ox ford, England) at eightfold dilution steps, starting with 1:1,000 and ending with 1:512,000 [10]. Antibody binding was visualized by a two-step immunofluorescence method based on affinity-purified biotinylated horse anti-mouse IgG (0.05 g IgG/l, 3 h) and fluores cein isothiocyanate (FITC)-labelled avidin (0.05 g/l, 30 min), both purchased from Vector Laboratories (Burlingame, Calif., USA) [II].…”

Section: Ige-positive Duodenal Mast Cellsmentioning

confidence: 99%

IgE-Positive Duodenal Mast Cells in Patients with Food-Related Diarrhea

Bengtsson¹,

Rognum

Brandtzæg

et al. 1991

Int Arch Allergy Immunol

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Thirty-seven consecutive adult patients with a history of adverse reactions to foods, manifested mainly as diarrhea, were investigated with skin prick test (SPT), IgE levels in serum, and the presence of IgE bound to mast cells in duodenal biopsy specimens. Nineteen percent had increased serum IgE levels indicating the presence of atopic disease and in 35% positive SPTs for one or several allergens related to their gastrointestinal symptoms were found. In 92% of the patients with positive SPTs to food, IgE-positive mast cells in duodenal biopsy specimens were found, twice as many as in patients with negative SPTs (47%). Forty-two percent of normal individuals without any adverse reactions to foods had IgE-bearing mast cells in their intestinal mucosa. The results showed that ‘arming’ of mast cells with IgE locally was relatively prominent but not consistent in the gut of patients with food-related diarrhea suggested to be allergic by positive SPT. Intestinal IgE-mediated hypersensitivity reactions could be of pathogenetic significance in most of these patients. However, since also half of the normal individuals were found to have IgE-positive intestinal mast cells, this phenomenon presumably also reflects a normal physiological defence mechanism.

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“…Untersmayr et al detected FcεRI-positive epithelial cells in the terminal ileum and the colon of colon cancer patients and patients with inflammatory conditions of the gut [20]. Previously, IgE-loaded mast cells have been described in the intestinal mucosa of food allergic- as well as healthy individuals [21], [22].…”

Section: Introductionmentioning

confidence: 99%

Fc-Epsilon-RI, the High Affinity IgE-Receptor, Is Robustly Expressed in the Upper Gastrointestinal Tract and Modulated by Mucosal Inflammation

et al. 2012

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BackgroundThe role of the high affinity IgE receptor, FcεRI, in IgE-mediated immune responses of the gastrointestinal (GI) mucosa is poorly understood. Currently, a detailed characterization of FcεRI expression throughout the human gut is lacking. The aim of this study was to define the expression pattern of FcεRI in the GI tract.Methods/Principal FindingsWe compared FcεRI expression in children with gastritis/esophagitis (n = 10), celiac disease (n = 10), inflammatory bowel disease (IBD) (n = 9), and normal mucosa (n = 5). The α–subunit of FcεRI (FcεRIα), detected by immunohistochemistry, was found on cells infiltrating the mucosa of the esophagus, the stomach, and the duodenum, but was rarely detected in more distal sections of the GI tract. Accordingly, quantitative RT-PCR analysis on esophagus, stomach, duodenum, colon, and rectum biopsies revealed that FcεRIα and -β expression levels decreased towards the distal intestine. mRNA transcripts of the common Fc-receptor-γ chain were present in the entire GI mucosa. Double-immunofluorescence staining of esophageal specimens confirmed that FcεRIα was expressed on intraepithelial mast cells and Langerhans cells. The mRNA expression levels of the α, β, and γ subunits of FcεRI did not correlate with total serum IgE but were associated with mucosal inflammation.Conclusion/SignificanceOur data define the upper GI tract as the main site for IgE-mediated immune activation via FcεRI. Tissue mRNA levels of FcεRIα are regulated by inflammatory conditions rather than serum IgE, indicating that FcεRI might also play a role in pathologies other than allergy.

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IgE-Positive Cells in Human Intestinal Mucosa Are Mainly Mast Cells

Cited by 27 publications

References 28 publications

Food intolerance and mucosal inflammation

Food intolerance and mucosal inflammation

IgE-Positive Duodenal Mast Cells in Patients with Food-Related Diarrhea

Fc-Epsilon-RI, the High Affinity IgE-Receptor, Is Robustly Expressed in the Upper Gastrointestinal Tract and Modulated by Mucosal Inflammation

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