Expression of a human alpha-1,3/4-fucosyltransferase in the pit cell lineage of FVB/N mouse stomach results in production of Leb-containing glycoconjugates: a potential transgenic mouse model for studying Helicobacter pylori infection.

Falk, Per; Bry, Lynn; Holgersson, Jan; Gordon, Jeffrey I.

doi:10.1073/pnas.92.5.1515

Cited by 125 publications

(106 citation statements)

References 14 publications

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“…Gastric biopsies were obtained from adult Peruvians who had clinical and endoscopic evidence of gastritis. The biopsies were used to confirm that they were Le b -positive (11) and to isolate H. pylori. Mascerated tissue samples were streaked on selective medium (Brain Heart Infusion agar containing 10% calf blood͞6 g͞ml vancomycin͞5 g͞ml trimethoprim͞8 g͞ml amphotericin B).…”

Section: Methodsmentioning

confidence: 99%

“…Transgenic mice were generated and genotyped as described (11). They were maintained, together with their normal littermates, in a specified pathogen free state and given Pico Lab Rodent Diet 20 (Purina Mills).…”

Section: Methodsmentioning

confidence: 99%

“…In vitro binding assays have shown that attachment to these cells can be mediated by epithelial receptors containing Le b (10). The was absent in all other gastric cell lineages (11). As described below, we have used this model to show that interactions between a bacterial adhesin and a host receptor can alter disease outcome in an animal without affecting colonization levels, thereby demonstrating that the mode of colonization can be crucial for pathogenesis.…”

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confidence: 99%

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Epithelial attachment alters the outcome of Helicobacter pylori infection

Guruge

Falk

Lorenz

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

269

167

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Genetically defined in vivo models are needed to assess the importance of target cell attachment in bacterial pathogenesis. Gastric colonization by Helicobacter pylori in human populations is common and persistent, and has various outcomes including peptic ulcers and cancer. The impact of attachment on the course of infection was examined in transgenic mice expressing a human receptor for H. pylori in their gastric epithelium. Persistent infection by a clinical isolate occurred at comparable microbial densities in transgenic and nontransgenic littermates. However, microbial attachment in transgenic mice resulted in production of autoantibodies to Lewis x carbohydrate epitopes shared by bacteria and acid-secreting parietal cells, chronic gastritis, and parietal cell loss. This model should help identify bacterial and host genes that produce attachment-related pathology.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Epithelial attachment alters the outcome of Helicobacter pylori infection

Guruge

Falk

Lorenz

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

269

167

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“…7) or by immunohistochemistry (data not shown). Expression is also silenced in the stomach: mucus-producing pit cells support expression of a variety of Fabpl Ϫ596 to ϩ21 /reporter transgenes (17,18), but immunoreactive hGH is not detectable in the pit cell or any other gastric epithelial lineage of Fabpl 4x at Ϫ132 / hGH animals (data not shown; cf. Fig.…”

Section: The 35-base Pair Element Can Function As a Suppressor Of Genmentioning

confidence: 99%

Suppressor and Activator Functions Mediated by a Repeated Heptad Sequence in the Liver Fatty Acid-binding Protein Gene (Fabpl)

Simon

Cho²,

Tso

et al. 1997

Journal of Biological Chemistry

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Epithelial cells that line the intestine and the nephrons of the kidney share many common functions. The molecular mechanisms that regulate gene transcription within and between these epithelia are largely uncharacterized. The "liver" fatty acid-binding protein gene (Fabpl) 1 provides a model for investigating these mechanisms.In the adult mouse and rat, Fabpl is transcribed in hepatocytes and in polarized absorptive enterocytes, the principal epithelial cell lineage of the small intestine (1). Fabpl exhibits a cephalocaudal gradient of expression within the intestine; highest levels of its mRNA and protein products are encountered in differentiated enterocytes that overlie villi located in the middle third of the small intestine; levels diminish as one moves proximally or distally. The gene is silent in the gastric and distal colonic epithelium of both species and in all other epithelia not associated with the gastrointestinal tract.The contribution of cis-acting suppressors to maintaining this pattern of expression was revealed from studies in transgenic mice (1). Seven fusion genes were produced by sequential deletions of the proximal 4000 nucleotides of rat Fabpl's 5Ј-nontranscribed domain and linkage of each truncated product to nucleotides ϩ3 to ϩ2150 of the human growth hormone (hGH) gene. The cellular and spatial patterns of expression of each fusion gene were defined in multiple pedigrees of adult

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“…In 1993, two studies showed that H pylori can bind to fucosylated glycoconjugates containing Le b structures on the surface of gastric epithelial cells within human biopsy specimens [4,5] . Studies using transgenic mice expressing the human Le b epitope in gastric epithelial cells indicated that Le b functions as a receptor for an H pylori-specific adhesin and mediates its attachment to the gastric pit and surface mucous cells [6] . Further studies using the same transgenic mice showed that H pylori was adherent to the surface of gastric epithelial cells, resulting in severe chronic gastric inflammation and atrophy; whereas H pylori was localized in the mucous layer in nontransgenic control mice [7] .…”

Section: Introductionmentioning

confidence: 99%