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The Role of Small Intestinal Permeab...

Arrieta Mendez, Marie-Claire.

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The Role of Small Intestinal Permeability in the Pathogenesis of Colitis in the Interleukin-10 Gene Deficient Mouse.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The Role of Small Intestinal Permeability in the Pathogenesis of Colitis in the Interleukin-10 Gene Deficient Mouse./
作者:	Arrieta Mendez, Marie-Claire.
面頁冊數:	178 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Contained By:	Dissertation Abstracts International72-08B.
標題:	Health Sciences, Pathology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR73256
ISBN:	9780494732564

The Role of Small Intestinal Permeability in the Pathogenesis of Colitis in the Interleukin-10 Gene Deficient Mouse.
Arrieta Mendez, Marie-Claire.

The Role of Small Intestinal Permeability in the Pathogenesis of Colitis in the Interleukin-10 Gene Deficient Mouse. - 178 p.

Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .

Thesis (Ph.D.)--University of Alberta (Canada), 2011.

It is currently believed that the etiology of inflammatory bowel disease involves an aberrant immune response towards the gastrointestinal microbial flora. In addition, an increase in intestinal paracellular permeability may also be a contributing factor of disease, as it precedes disease in several animal models. However, it remains unclear whether increased intestinal permeability is an epiphenomenon of disease or if it can lead to it. The goal of this thesis is to elucidate this cause-effect relationship.

ISBN: 9780494732564Subjects--Topical Terms:

1017854
Health Sciences, Pathology.

The Role of Small Intestinal Permeability in the Pathogenesis of Colitis in the Interleukin-10 Gene Deficient Mouse.
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520 $a It is currently believed that the etiology of inflammatory bowel disease involves an aberrant immune response towards the gastrointestinal microbial flora. In addition, an increase in intestinal paracellular permeability may also be a contributing factor of disease, as it precedes disease in several animal models. However, it remains unclear whether increased intestinal permeability is an epiphenomenon of disease or if it can lead to it. The goal of this thesis is to elucidate this cause-effect relationship.
520 $a The IL-10-/- mouse is a model of IBD that spontaneously develops colitis after 12 weeks of age. We measured intestinal permeability in this mouse from 4-17 weeks of age and observed that there was a significant increase in small intestinal permeability early in life and before the onset of colitis.
520 $a When small intestinal permeability was selectively decreased with AT-1001 (a ZOT antagonist peptide) colitis was significantly ameliorated. In contrast, when it was increased with AT-1002 (a ZOT agonist peptide) colitis worsened, indicating that modifications in the paracellular traffic of the small intestine had a significant effect on the severity of colonic disease.
520 $a In order to study the possible mechanisms by which small intestinal permeability modulated disease in the colon, we measured the effect of increasing small intestinal permeability on the colonic microbial flora of IL-10-/- mice. After AT-1002 treatment from 4-12 weeks of age, there was an evident shift in colonic adherent flora. This effect was not a consequence of inflammation as there was a similar effect in wild type mice.
520 $a We also studied the effect of increasing small intestinal permeability in the development of oral tolerance to dietary antigens. When wild-type mice were fed OVA under conditions of increased small intestinal permeability there was a significant increase in the proliferation of B cells in the spleen and an increase in OVA-specific humoral response, compared to animals fed OVA alone. Moreover, the production of IL-10 in response to oral OVA was prevented when OVA was given with AT-1002, both in the small intestine and the colon.
520 $a The studies presented in the doctoral thesis suggest that small intestinal permeability has a critical role in the development of colitis in IL-10-/-mice, and that increasing paracellular traffic in the small intestine may lead to changes in colonic bacterial flora and the abrogation of tolerance to oral antigens, two features of inflammatory bowel disease in humans.
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