Helicobacter pylori and peptic ulcers: the present position.

Moss, Steven F.; Calam, J.

doi:10.1136/gut.33.3.289

Cited by 131 publications

(51 citation statements)

References 59 publications

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“…Although the physiologic significance of H. pylori in the parietal cell canaliculi is not yet clear, several reports demonstrate that H. pylori infection is responsible for alterations in gastric physiology. 53 The findings of the present study indicate that H. pylori does invade the gastric mucosa and translocates to the gastric lymph nodes. The observation of many H. pylori captured by macrophages in the lamina propria as well as in the lymph nodes suggests that H. pylori-specific T cells can be primed and maintained within these regions.…”

Section: Intestinal Metaplasiamentioning

confidence: 69%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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Helicobacter pylori has been considered to be non-invasive and to rarely infiltrate the gastric mucosa, even though there is an active Th1 immune response in the lamina propria of the H. pylori-infected stomach. To elucidate whether H. pylori invades the lamina propria and translocates to the gastric lymph nodes, we examined H. pylori in formalin-fixed and paraffin-embedded tissue sections of stomach and gastric lymph nodes obtained from 51 cancer patients using real-time PCR and immunohistochemistry (IHC) with a novel anti-H. pylori monoclonal antibody that recognizes lipopolysaccharides. Fresh gastric lymph nodes were used to culture for H. pylori. In 46 patients with H. pylori in the stomach, the bacterium was found in the lymph nodes from 21 patients by culture, 37 patients by PCR, and 29 patients by IHC. H. pylori captured by macrophages was found in the lamina propria of 39 patients. In the lymph nodes, the bacterium was found in many macrophages and a few interdigitating dendritic cells at the paracortical areas. H. pylori was also found in the intracellular canaliculi of parietal cells in 21 patients, but intracytoplasmic invasion into gastric epithelial cells was not identified. When compared to the commercially available anti-H. pylori antibodies, the novel antibody showed the highest sensitivity to detect H. pylori-positive macrophages, whereas no difference was found for H. pylori in the mucous layer. The H. pylori-positive macrophages in the lamina propria correlated with chronic gastritis as well as translocation of such cells to the lymph nodes. These results suggest that H. pylori-induced gastric epithelial damage allows the bacteria to invade the lamina propria and translocate to the gastric lymph nodes, which may chronically stimulate the immune system. The bacteria captured by macrophages, whether remaining alive or not, may contribute to the induction and development of H. pylori-induced chronic gastritis.

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Section: Intestinal Metaplasiamentioning

confidence: 69%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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“…H. pylori is now recognized as one of the most common bacterial infections in humans. It has been connected with the onset of gastritis and peptic ulcer disease [31,32] and has been implicated as a contributing factor in gastric cancer [33]. We now report the isolation of the DHQase from H. pylori.…”

Section: Introductionmentioning

confidence: 93%

Cloning, sequencing, expression, purification and preliminary characterization of a type II dehydroquinase from Helicobacter pylori

Bottomley

Clayton²,

Chalk³

et al. 1996

Biochemical Journal

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A heat-stable dehydroquinase was purified to near homogeneity from a plate-grown suspension of the Gram-negative stomach pathogen Helicobacter pylori, and shown from both its subunit and native molecular masses to be a member of the type II family of dehydroquinases. This was confirmed by N-terminal amino acid sequence data. The gene encoding this activity was isolated following initial identification, by random sequencing of the H. pylori genome, of a 96 bp fragment, the translated sequence of which showed strong identity to a C-terminal region of other type II enzymes. Southern blot analysis of a cosmid library identified several potential clones, one of which complemented an Escherichia coliaroD point mutant strain deficient in host dehydroquinase. The gene encoding the H. pylori type II dehydroquinase (designated aroQ) was sequenced. The translated sequence was identical to the N-terminal sequence obtained directly from the purified protein, and showed strong identity to other members of the type II family of dehydroquinases. The enzyme was readily expressed in E. coli from a plasmid construct from which several milligrams of protein could be isolated, and the molecular mass of the protein was confirmed by electrospray MS. The aroQ gene in H. pylori may function in the central biosynthetic shikimate pathway of this bacterium, thus opening the way for the construction of attenuated strains as potential vaccines as well as offering a new target for selective enzyme inhibition.

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“…A strong association between Helicobacter pylori and chronic active inflammation of the gastric antrum and duodenal ulceration has been recognized (4,14,(20)(21)(22). Several therapeutic regimens have been proposed to clear H. pylori infections and to obtain a long-term eradication of the microorganism (6,9,15,17).…”

mentioning

confidence: 99%

Helicobacter pylori: A Fickle Germ

Cellini

Allocati

Campli

et al. 1994

Microbiology and Immunology

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The morphologic changes from bacillary to coccoid forms of Helicobacter pylori were studied. These form changes were analyzed by bacterial growth in Brucella broth plus 2% fetal calf serum. The coccoid forms were observed at five days of incubation and a rapid decrease of CFU/ml was recorded. At two weeks of microaerophilic incubation, all coccoid forms observed were not culturable in vitro. The coccoid morphology was observed earlier when the culture of H. pylori was incubated in aerobic conditions and with subinhibitory concentrations of omeprazole and roxithromycin. To evaluate the possibility of resistance of coccal forms, before plating, the cultures were heated to 80 C for 10 min and sonicated. In the absence of these treatments the cultures did not show growth in vitro. The proteic patterns of the same strains of two different morphologies were studied revealing significant differences.

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Helicobacter pylori and peptic ulcers: the present position.

Cited by 131 publications

References 59 publications

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Cloning, sequencing, expression, purification and preliminary characterization of a type II dehydroquinase from Helicobacter pylori

Helicobacter pylori: A Fickle Germ

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