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Chapter 45 : In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases

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Abstract:

The presence of spp. in the gastric mucosa is associated with inflammation and/or ulceration, and these bacteria are recognized as important pathogens in gastroduodenal disease. There is now mounting evidence that suggests that enterohepatic spp. may also be pathogenic for the host. Various other gastric spp. have now been isolated and characterized. Indeed, in rhesus and cynomolgus monkeys, these gastric spp. are indistinguishable from , whereas pig-tailed macaques are colonized by . Several experimental models have been developed to study the inflammatory processes induced by the murine enterohepatic spp. As , induces the proliferation of intestinal and hepatic host cells in vivo, it is unlikely that enterocytes or hepatocytes are the target cells for cytolethal distending toxin (Cdt). Recently, studies in SS1-infected mice demonstrated that infection models could also be used to address questions relating to the development of antimicrobial resistance in in vivo and to the study of the molecular mechanisms involved in resistance. In common with human -associated gastritis, the local inflammatory infiltrates in infected animal hosts are characterized by the presence of large CD3 T-lymphocyte populations, the majority of which have a CD4 phenotype.

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45

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Figure 1

Experimental gastric Helicobacter infections in mice. Panels A and B show gastric tissue sections from mice infected with the SSI strain (arrows). Large numbers of bacteria are seen colonizing the lumen of the gastric glands (Warthin-Starry silver-stain). Panels C and D show mild inflammatory lesions composed of mononuclear cell infiltrates (asterisks) in the submucosa and superficial areas of the gastric mucosa from mice with an infection (4 months after inoculation; hematoxylin and eosin). Panels E and F show severe inflammation in mice with chronic infection (13 months after inoculation). The figures depict two types of host-dependent gastritis in mice, characterized by (E) lymphoid cell aggregate formation (asterisk) and reorganization of gastric gland architecture and (F) epithelial hyperplasia and glandular atrophy (hematoxylin and eosin). (From collaborative work with the Unite de Histopathologic, Institut Pasteur, Paris.)

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45
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Image of Figure 2
Figure 2

Extragastric spp. and the induction of hepatic inflammatory lesions in mice. (A) A transmission electron micrograph shows the distinctive spiral morphology and bipolar flagella of Light micrographs depict (B) organisms (arrows) in mouse liver (Warthin-Starry silver-stain) and (C) a focus of mononuclear cell infiltration in a mouse liver (hematoxylin and eosin).

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45
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Figure 3

Bacterium-host cell interactions during gastric helicobacter infection. Transmission electron photomicrographs show (A) (B) (C) and (D) bacteria (arrows) in the gastric mucosae of experimentally infected mice (A, B, C) and naturally infected ferrets (D), respectively. The bacteria (arrows) can be observed to be either distant to (A, C) or intimately associated with (B, D) the mucosa. (Original photomicrographs kindly provided by J. L. O'Rourke, University of New South Wales, Sydney.)

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45
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Tables

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Table 1

The principal pathogenic spp., their hosts, and the diseases caused

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45
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Table 2

Experimental parameters to consider when establishing an mouse infection model

Citation: Ferrero R, Fox J. 2001. In Vivo Modeling of Helicobacter-Associated Gastrointestinal Diseases, p 565-582. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch45

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