Quantitative Analysis of Small Intestinal Mucosa in Cowʼs Milk-Sensitive Enteropathy

Maluenda, Carlos; Ad, Phillips; Briddon, A.; Ja, Walker-Smith

doi:10.1097/00005176-198406000-00008

Cited by 95 publications

(32 citation statements)

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“…The intestinal tissue of this animal model exhibits loss of villous architecture together with a characteristic feature of tissue repair, where specific IgE and degranulating IgE-positive mast cells, as well as antigen-specific T cells, were functional. Pathological changes were similar to results of studies on tissues collected from patients with food-sensitive enteropathy, [18][19][20][21] in that an increase in mucosal IgE secreting plasma cells and degranulating mast cells in the jejunum were described. 20 In addition, in relation to the large intestine, although this model lacked features such as diarrhea and morphologic changes observed in other models of food-induced colitis, 5-7 the pathology was consistent with that examined in tissues from patients with intestinal food allergies.…”

Section: Discussionsupporting

confidence: 81%

Food antigen causes TH2-dependent enteropathy followed by tissue repair in T-cell receptor transgenic mice

Nakajima‐Adachi

Ebihara

Kikuchi

et al. 2006

Journal of Allergy and Clinical Immunology

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Section: Discussionsupporting

confidence: 81%

Food antigen causes TH2-dependent enteropathy followed by tissue repair in T-cell receptor transgenic mice

Nakajima‐Adachi

Ebihara

Kikuchi

et al. 2006

Journal of Allergy and Clinical Immunology

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“…Measurement of villous height and crypt depth was performed as previously described (23). Wellorientated crypt-villous units were measured (ϫ400 magnification) using Imagan 2 software (Kompira, U.K.).…”

Section: Methodsmentioning

confidence: 99%

Chronic T Cell-Mediated Enteropathy in Rural West African Children: Relationship with Nutritional Status and Small Bowel Function

et al. 2003

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Previous studies from The Gambia have shown that poor childhood growth is resistant to all but the most intense nutritional intervention and highly dependent on small bowel permeability related to enteropathy. We thus aimed to characterize the mucosal inflammatory response in rural Gambian children in relation to intestinal permeability and nutritional status. Small bowel biopsies were taken from 38 rural Gambian children (age, 0.5-3 y) with a range of nutritional and clinical states (median weight z score, Ϫ4.6; range, 0.5 to Ϫ6.4), 75% of whom had diarrhea. Morphometry was performed with immunohistochemical analysis for a range of lineage and activation markers, including proinflammatory and regulatory cytokines, and related to current clinical status and gut permeability. Comparison was made with 19 age-matched U.K. controls. All Gambian children, regardless of nutritional status, had evidence of chronic cellmediated enteropathy with crypt hyperplasia, villous stunting, and high numbers of intraepithelial lymphocytes. CD25ϩ cells were 20-fold higher than in U.K. controls. Although small bowel architecture was independent of nutritional status, T cell numbers rose and B cell numbers fell with worsening nutrition, and mucosal cytokine production became biased toward a proinflammatory response, with progressive decrease of transforming growth factor-␤ expression. Tropical enteropathy predates the onset of marasmus and is characterized by a cell-mediated T H 1 response. Protein-energy malnutrition is associated with reduction of regulatory immune responses in the mucosal microenvironment, potentially impairing the mechanisms of oral tolerance. Children from The Gambia show a pattern of growth faltering typical of deprived areas of the developing world (1-4). Growth velocity falls from 4 mo onward, so by age 2, the mean weight-for-age lies 2 SD below U.K. standards (z score, Ϫ2). Previous studies from Keneba, rural Gambia, have identified biochemical and dietary deficiencies in these infants. Despite seemingly well-targeted nutritional intervention with macroand micronutrients, growth faltering continues (5-9). Massive dietary supplementation (twice recommended values for energy, 2.5 times for protein) produced short-term catch-up growth after gastroenteritis (5), but growth acceleration reached only the population mean, still 2 SD below the U.K., and reversed as soon as the child left the refeeding study (1, 8).The failure of dietary intervention to restore growth has led to search for other factors. Quantitatively the most important association identified is small bowel enteropathy (2, 4, 10), demonstrated by lactulose:mannitol (L:M) dual sugar permeability testing (11). This assesses both epithelial integrity (exclusion of lactulose entry through intercellular tight junctions) and absorptive capacity (passive absorption of mannitol) (12). During a 1-y period, increased L:M ratio accounted for 0031-3998/03/5403-0306 PEDIATRIC RESEARCH Vol. 54, No. 3, 2003 Copyright © 2003 Printed in U.S.A. ABSTRACT306

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“…Whole sections of tissues were assessed morphometrically using the methods of Maluenda et al 25 Haematoxylin and eosin and PAS stained sections were examined at a total magnification of 116 times using a drawing arm attachment on an Olympus BMB light microscope. Only well orientated sections were studied and care was taken to ensure that only longitudinal sections cut perpendicularly to the muscularis mucosae were included.…”

Section: Morphometrymentioning

confidence: 99%

Sequential changes in small intestinal structure and function during rotavirus infection in neonatal rats.

Salim

Phillips

Walker-Smith

et al. 1995

Gut

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Rotavirus infection is the most common cause of acute diarrhoea in children worldwide. The structural and functional consequences of mammalian rotavirus infection in the small intestine have been incompletely studied and the mechanism of enterocyte damage poorly defined. This The pathophysiology of rotavirus diarrhoea, has been studied only in neonatal pigs20-21 and mice.22 The neonatal pig model has been used for both in vivo21 and in vitro20 studies.Rotavirus infected neonatal mouse intestine has been studied in vitro using isolated intestinal segments without an intact blood and nerve supply22 and thus the pathophysiological relevance of this model might be questioned.Recently, a group B rotavirus has been reported to cause symptomatic diarrhoea in neonatal rats23 and a similar virus can cause diarrhoea in humans.24 We have infected neonatal rats with group B rat rotavirus and related the clinical course of diarrhoea to virus excretion in faeces, and to structural and functional abnormalities in the small intestine. This is the first systematic characterisation of this rotavirus infection in neonatal rats, which we consider will prove to be an excellent model for studying pathogenesis of human rotavirus infection. Methods ANIMALSNeonatal rats (Bantin & Kingham Ltd, Aldbrough Hill, UK) were obtained at the age of 5 days. For the three days before inoculation, they were kept with their mother and allowed to suckle ad libitum. At the time of inoculation each animal was about 6 cm long and weighed 12-15 g. At least six to eight animals were studied in each group at each time point.

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Quantitative Analysis of Small Intestinal Mucosa in Cowʼs Milk-Sensitive Enteropathy

Cited by 95 publications

References 0 publications

Food antigen causes TH2-dependent enteropathy followed by tissue repair in T-cell receptor transgenic mice

Food antigen causes TH2-dependent enteropathy followed by tissue repair in T-cell receptor transgenic mice

Chronic T Cell-Mediated Enteropathy in Rural West African Children: Relationship with Nutritional Status and Small Bowel Function

Sequential changes in small intestinal structure and function during rotavirus infection in neonatal rats.

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