Deposition of eosinophil-granule major basic protein and expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the mucosa of the small intestine in infants with cow’s milk–sensitive enteropathy

Chung, Hai Lee; Hwang, Jin Bok; Kwon, Young Dae; Park, Min Ho; Shin, Won Jeong; Park, Jae Bok

doi:10.1016/s0091-6749(99)70199-5

Cited by 53 publications

(43 citation statements)

References 23 publications

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“…On the other hand, we did not find evidence that either ICAM-1 or VCAM-1 is involved in T lymphocyte migration in the small intestine. Several studies (7,11,33) on food allergy and animal models have suggested that the increased expression of ICAM-1 or VCAM-1 is related to the pathogenesis of leukocyte infiltration to the intestinal mucosa. We surmise that leukocyte subpopulations other than T cells, such as neutrophils, might play important roles via an ICAM-1-dependent mechanism in these situations.…”

Section: Discussionmentioning

confidence: 99%

“…Studies of other atopic diseases and animal models suggest that adhesion molecules and mucosal lymphocytes are implicated in the pathogenesis of food allergy (12). Several clinical reports (7,33) have also indicated that the expression of adhesion molecules is increased in the duodenal mucosa of adult patients with food allergies or of infants with cow's milk-sensitive enteropathy. However, only a few studies have addressed lymphocyte trafficking in food allergies, and the mechanisms of directly "trafficking" cells have only scarcely been explored (11,28).…”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

mentioning

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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“…Subsequently, the permeability of the gut could be enhanced, and the antigenic load could thereby increase. It has been demonstrated in previous studies that eosinophils and their mediators may have a role in the intestinal inflammation process (27)(28)(29)(30). Chung and colleagues (27) have demonstrated elevated levels of eosinophil-derived major basic protein in the intestinal mucosa of infants with cow's milksensitive enteropathy, but they had no evidence about the original source of the major basic protein.…”

Section: Breast Milk Ecp In Cow's Milk Allergymentioning

confidence: 99%

“…It has been demonstrated in previous studies that eosinophils and their mediators may have a role in the intestinal inflammation process (27)(28)(29)(30). Chung and colleagues (27) have demonstrated elevated levels of eosinophil-derived major basic protein in the intestinal mucosa of infants with cow's milksensitive enteropathy, but they had no evidence about the original source of the major basic protein. Eosinophilic gastroenteritis is characterized by a pronounced intestinal eosinophil accumulation and activation, and the eosinophilic activation is reported to directly reflect to the fecal ECP levels (31).…”

Section: Breast Milk Ecp In Cow's Milk Allergymentioning

confidence: 99%

Eosinophil Cationic Protein in Human Milk Is Associated with Development of Cow's Milk Allergy and Atopic Eczema in Breast-fed Infants

et al. 2004

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The precise role of leukocytes and mediators in human milk is still unresolved. Eosinophils are uncommonly detected in human milk and their presence has previously been associated with maternal atopy and development of cow's milk allergy (CMA) in the breast-fed infant. The purpose of this study was to examine the levels of eosinophil cationic protein (ECP) in human milk and to compare the levels with development of allergic diseases in breast-fed infants. Altogether 94 breast-feeding mothers (58 atopic, 36 nonatopic) with their babies were prospectively followed from birth for development of CMA or atopic dermatitis. Colostrum and mature milk samples (at 3 mo of lactation), together with mother's peripheral blood samples, were collected. Milk and blood leukocyte content was evaluated with a light microscope. ECP concentration in human milk was measured by commercial UniCAP method. By the end of a 2-y follow-up, 51 mothers had an infant with CMA, 24 had an infant with atopic dermatitis, and 19 had a healthy infant. ECP concentration in milk was under the detection limit (2 g/L) in all the mothers with a healthy infant, whereas detectable levels were found in 27% of mothers with a CMA infant and in 42% of those with a baby with atopic dermatitis. Measurable ECP in milk was detected in 26% of the atopic and 25% of the nonatopic mothers. Presence of ECP in human milk is associated with development of CMA and atopic dermatitis in the breast-fed infant, but has no direct association with the maternal atopy. Human breast milk provides nutrients and multiple immunologic factors, like secretory IgA, to the breast-fed infant (1). It is known to be an important immunologic support system extending from the mother to her infant during the first months of life. The precise role of leukocytes in human milk is still unknown. In animal studies, milk leukocytes have been shown to pass through the gastrointestinal mucosa of a suckling newborn (2-5). They produce cytokines and mediators, which may be released throughout the gastrointestinal tract (6). In our previous studies, we have found that macrophage is the predominant leukocyte in milk of mothers with a healthy baby, whereas in the mothers with a CMA infant, neutrophils and eosinophils are found in excess (7). We have also shown that decreased function of macrophages is likewise associated with development of CMA in breast-fed infants (8), suggesting that defective immunologic support from mother's milk may interfere with normal development of oral tolerance to food proteins.Eosinophils are mainly tissue-dwelling cells. The bloodtissue ratio of eosinophils has been estimated to be 1:100 (9) Eosinophils are presumably involved in normal immune defense as well as in specific morbid processes including parasitic infections and hypersensitivity reactions (9, 10). Eosinophil granules contain cationic proteins, which have been demonstrated in vivo and in vitro to be tissue-destructive (9). Detection of eosinophil-derived granular proteins reflects earlier degranulation of eosinoph...

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“…FPIES is classified as a cellmediated disorder presumed to involve antigen-specific T lymphocytes, monocytes, antibodies, and cytokines as a cause of inflammation in the colon and, with variable degrees, the ileum [70,[91][92][93][94][95][96][97]. This inflammation is hypothesized to result in increased intestinal permeability leading to a fluid shift into the gastrointestinal lumen.…”

Section: Pathophysiologymentioning

confidence: 99%

Food Protein–Induced Enterocolitis Syndrome

Nowak‐Węgrzyn

Jarocka-Cyrta

Castro

2017

J Investig Allergol Clin Immunol

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Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-, cell-mediated food allergy of unknown prevalence and pathophysiology. Onset is typically during the first year of life; seafood-induced FPIES may start in adulthood. Acute FPIES manifests within 1-4 hours after ingestion with repetitive emesis, pallor, and lethargy progressing to dehydration and hypovolemic shock in 15% of cases. Chronic FPIES manifests with intermittent emesis, watery diarrhea, and poor growth progressing to dehydration and hypovolemic shock over a period of days to weeks. Chronic FPIES has been only reported in infants aged less than 3 months fed with cow milk (CM) or soy formula. The most common triggers are CM, soy, rice, and oat. Diagnosis of FPIES relies on recognition of a pattern of clinical symptoms and may be missed owing to the absence of typical allergic symptoms (eg, urticaria, wheezing) and delayed onset in relation to food ingestion. Physician-supervised food challenge is recommended if diagnosis or the trigger food is not clear and to evaluate for resolution. Testing for food-specific IgE is usually negative, although a subset of patients, usually with CM-induced FPIES may develop sensitization to foods. Such atypical FPIES tends to have a more prolonged course. Despite the potential severity of the reactions, no fatalities have been reported, and FPIES has a favorable prognosis. In most cases, FPIES resolves by age 3-5 years, although persistence of CM-induced FPIES and soy FPIES into adulthood has been reported. The first international consensus guidelines on diagnosis and management of FPIES were published in 2017. Given that the pathophysiology of FPIES is poorly understood, there are no diagnostic biomarkers and no therapies to accelerate resolution. These unmet needs warrant future investigations to improve the care of patients with FPIES. Key words: FPIES. Food protein-induced enterocolitis syndrome. Non-IgE-mediated food allergy. Food allergy. Cow milk allergy. ResumenSEIOA es una alergia alimentaria con patofisiología y prevalencia desconocidas, que típicamente comienza en el primer año de vida, mientras que la producida por pescado suelo tener su comienzo en adultos. La forma aguda se manifiesta entre la hora y 4 horas tras la ingesta del alimento con emesis, palidez, letargia progresiva por deshidratación y shock hipovolémico en el 15% de los casos. La forma crónica se manifiesta con emesis intermitente, diarreas y crecimiento pobre con progresión hacia la deshidratación y shock hipovolémico en un periodo de días o semanas. La forma crónica se ha podido observar únicamente en niños menores de 3 años alimentados con leche de vaca o fórmula de soja. Los desencadenantes más frecuentes son la leche de vaca, la soja, el arroz y avena. El diagnóstico es clínico y puede ser difícil debido a la ausencia de síntomas alérgicos típicos (urticaria, asma…) y a la relación retardada con la ingesta. Es recomendable la provocación controlada si el diagnóstico clínico o el alimento implicado no son claros y tamb...

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Deposition of eosinophil-granule major basic protein and expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the mucosa of the small intestine in infants with cow’s milk–sensitive enteropathy

Cited by 53 publications

References 23 publications

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

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

Eosinophil Cationic Protein in Human Milk Is Associated with Development of Cow's Milk Allergy and Atopic Eczema in Breast-fed Infants

Food Protein–Induced Enterocolitis Syndrome

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