Duodenal mucosal damage in 31 infants with gastroenteritis

Barnes, Graeme L.; Townley, R. R. W.

doi:10.1136/adc.48.5.343

Cited by 137 publications

(60 citation statements)

References 11 publications

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“…Of course, in the absence of electron microscopy, it is not possible to be certain that the epithelium of the mucosa was completely normal morphologically in the three children who had normal histology, despite reduced lactase levels. Barnes and Townley (1973) reported similar findings in biopsies from children with acute gastroenteritis, and they also showed that acute disaccharidase depression did not correlate with subsequent persisting lactose intolerance. It is also known that lactase activities vary according to the site within the small intestine from which they are taken, the levels being higher in the jejunum than in the duodenum (Dahlqvist, 1964).…”

Section: Discussionmentioning

confidence: 55%

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Harrison¹,

Walker-Smith²

1977

Gut

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SUMMARY Thirty children on a lactose-free diet aged from 2-38 months who had previously been diagnosed as having secondary lactose intolerance were reinvestigated on 32 occasions by an oral lactose tolerance test, small intestinal biopsy, and measurement of disaccharidase activity in order to detect the presence of continuing lactose intolerance before reintroduction of milk. No correlation was found between continuing lactose intolerance, as diagnosed by the development of watery stools containing excess reducing substances after an oral load of lactose, and maximum blood glucose rise during a lactose tolerance test, lactase levels, and small intestinal morphology.

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Section: Discussionmentioning

confidence: 55%

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Harrison¹,

Walker-Smith²

1977

Gut

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“…In this study, Gn pigs inoculated with a heterologous virulent rotavirus (virulent Wa HRV) developed clinical signs and lesions characteristic of homologous virulent rotavirus infections in children (Bishop et aI., 1973;Barnes & Townley, 1973;Davidson & Barnes, 1979;Korting & Fiehring, 1983), pigs (Collins et al, 1989;Theil eta]., 1978; McAdaragh et a]., 1980), lambs (Snodgrass eta]., 1977), calves (Hall et aI., 1993;Castrucci et al, 1983) and mice (Adams & Kraft, 1967;Pappenheimer & Enders, 1947). The occurrence of diarrhoea and morphological lesions following HRV infection has been reported before in heterologous hosts, but only in Gn calves (Mebus et al,I977) and neonatal mice (Gouvea et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of an attenuated and a virulent strain of group A human rotavirus in neonatal gnotobiotic pigs

Ward

Rosen

Yuan

et al. 1996

Journal of General Virology

133

146

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“…Infection with G. duodenalis provides an interesting model for studying mucosal immunity, as some of the immunopathology observed in human patients and infected animals resembles that of common noninfectious intestinal disorders. The reduction of intestinal disaccharidase enzymes, for example, is a pathological hallmark of giardiasis and is also commonly observed in gastroenteritis, celiac disease, ulcerative colitis, and Crohn's disease patients (1)(2)(3)(4). Therefore, there are likely overlapping mechanisms involved.…”

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confidence: 99%

The Microbiota Contributes to CD8⁺T Cell Activation and Nutrient Malabsorption following Intestinal Infection with Giardia duodenalis

Keselman

Maloney

et al. 2016

Infect Immun

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Giardia duodenalis is a noninvasive luminal pathogen that impairs digestive function in its host in part by reducing intestinal disaccharidase activity. This enzyme deficiency has been shown in mice to require CD8 ؉ T cells. We recently showed that both host immune responses and parasite strain affected disaccharidase levels during murine giardiasis. However, high doses of antibiotics were used to facilitate infections in that study, and we therefore decided to systematically examine the effects of antibiotic use on pathogenesis and immune responses in the mouse model of giardiasis. We found that antibiotic treatment did not overtly increase the parasite burden but significantly limited the disaccharidase deficiency observed in infected mice. Moreover, while infected mice had more activated CD8 ؉ ␣␤ T cells in the small intestinal lamina propria, this increase was absent in antibiotictreated mice. Infection also led to increased numbers of CD4 ؉ ␣␤ T cells in the lamina propria and activation of T cell receptor ␥␦-expressing intraepithelial lymphocytes (IEL), but these changes were not affected by antibiotics. Finally, we show that activated CD8؉ T cells express gamma interferon (IFN-␥) and granzymes but that granzymes are not required for sucrase deficiency. We conclude that CD8؉ T cells become activated in giardiasis through an antibiotic-sensitive process and contribute to reduced sucrase activity. These are the first data directly demonstrating activation of CD8؉ T cells and ␥␦ T cells during Giardia infections. These data also demonstrate that disruption of the intestinal microbiota by antibiotic treatment prevents pathological CD8 ؉ T cell activation in giardiasis.T he protozoan Giardia duodenalis is a major cause of parasitic diarrheal disease worldwide. Infection with G. duodenalis provides an interesting model for studying mucosal immunity, as some of the immunopathology observed in human patients and infected animals resembles that of common noninfectious intestinal disorders. The reduction of intestinal disaccharidase enzymes, for example, is a pathological hallmark of giardiasis and is also commonly observed in gastroenteritis, celiac disease, ulcerative colitis, and Crohn's disease patients (1-4). Therefore, there are likely overlapping mechanisms involved. The reduction of disaccharidase enzymes in giardiasis results from a shortening of the intestinal epithelial microvilli structures and reflects a general impairment of digestion and nutrient absorption (5-7). We have demonstrated that wild-type mice exhibit reduced disaccharidase activity following infection with G. duodenalis but that CD4Another study has demonstrated that the adoptive transfer of purified CD8 ϩ T cells, but not CD4 ϩ T cells, from Giardia muris-infected mice into athymic naive recipients is sufficient to recapitulate shortening of microvilli and intestinal disaccharidase reduction (7). Collectively, these data suggest that CD8 ϩ T cells are involved in the pathological reduction of intestinal disaccharidases following infection...

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Duodenal mucosal damage in 31 infants with gastroenteritis

Cited by 137 publications

References 11 publications

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Pathogenesis of an attenuated and a virulent strain of group A human rotavirus in neonatal gnotobiotic pigs

The Microbiota Contributes to CD8⁺T Cell Activation and Nutrient Malabsorption following Intestinal Infection with Giardia duodenalis

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Duodenal mucosal damage in 31 infants with gastroenteritis

Cited by 137 publications

References 11 publications

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Pathogenesis of an attenuated and a virulent strain of group A human rotavirus in neonatal gnotobiotic pigs

The Microbiota Contributes to CD8+T Cell Activation and Nutrient Malabsorption following Intestinal Infection with Giardia duodenalis

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The Microbiota Contributes to CD8⁺T Cell Activation and Nutrient Malabsorption following Intestinal Infection with Giardia duodenalis