Helicobacter pylori and gastric acid: Biological and therapeutic implications

McGowan, Catherine C.; Cover, Timothy L.; Blaser, Martin J.

doi:10.1053/gast.1996.v110.pm8608904

Cited by 204 publications

(117 citation statements)

References 12 publications

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“…The gramnegative bacterium Helicobacter pylori, which is the major cause of chronic gastritis [1], peptic ulcer disease [2], gastric cancer and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach [3], is an exception to this rule. During infection associated with gastritis, the majority of H. pylori are found as bacilli attached to the surface of the epithelial cells of the gastric mucosa [4,5].…”

Section: Introductionmentioning

confidence: 99%

Profiling of bacterial flora in gastric biopsies from patients with Helicobacter pylori-associated gastritis and histologically normal control individuals by temperature gradient gel electrophoresis and 16S rDNA sequence analysis

Monstein¹,

Tiveljung²,

Kraft³

et al. 2000

Journal of Medical Microbiology

107

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Section: Introductionmentioning

confidence: 99%

Profiling of bacterial flora in gastric biopsies from patients with Helicobacter pylori-associated gastritis and histologically normal control individuals by temperature gradient gel electrophoresis and 16S rDNA sequence analysis

Monstein¹,

Tiveljung²,

Kraft³

et al. 2000

Journal of Medical Microbiology

107

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“…These are two distinct aspects of acid resistance. In H. pylori, survival under conditions of acid shock is largely mediated by urea uptake and its breakdown by urease (52,55). However, growth of H. pylori at low pH does not depend on urease activity (9,10) and requires genes such as lepA, uvrA, atpF, the flavin reductase gene, czcA, and aldo-keto reductase (10), some of which were not previously known to play a role in acid resistance.…”

mentioning

confidence: 99%

Identification of Campylobacter jejuni Genes Contributing to Acid Adaptation by Transcriptional Profiling and Genome-Wide Mutagenesis

Reid

Pandey

Palyada

et al. 2008

Appl Environ Microbiol

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In order to cause disease, the food-and waterborne pathogen Campylobacter jejuni must face the extreme acidity of the host stomach as well as cope with pH fluctuations in the intestine. In the present study, C. jejuni NCTC 11168 was grown under mildly acidic conditions mimicking those encountered in the intestine. The resulting transcriptional profiles revealed how this bacterium fine-tunes gene expression in response to acid stress. This adaptation involves the differential expression of respiratory pathways, the induction of genes for phosphate transport, and the repression of energy generation and intermediary metabolism genes. We also generated and screened a transposon-based mutant library to identify genes required for wild-type levels of growth under mildly acidic conditions. This screen highlighted the important role played by cell surface components (flagella, the outer membrane, capsular polysaccharides, and lipooligosaccharides) in the acid stress response of C. jejuni. Our data also revealed that a limited correlation exists between genes required for growth under acidic conditions and genes differentially expressed in response to acid. To gain a comprehensive picture of the acid stress response of C. jejuni, we merged transcriptional profiles obtained from acid-adapted cells and cells subjected to acid shock. Genes encoding the transcriptional regulator PerR and putative oxidoreductase subunits Cj0414 and Cj0415 were among the few up-regulated under both acid stress conditions. As a Cj0415 mutant was acid sensitive, it is likely that these genes are crucial to the acid stress response of C. jejuni and consequently are important for host colonization.

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“…The natural history of colonization involves an initial period of rapid bacterial growth associated with gastritis and reduced acid production. In most hosts, the inflammatory response diminishes within several months, leaving an asymptomatic diffuse gastritis with normal acid production that persists for years (2,3). A subpopulation of colonized individuals develops peptic ulcers (4).…”

mentioning

confidence: 99%

Epithelial attachment alters the outcome of Helicobacter pylori infection

Guruge

Falk

Lorenz

et al. 1998

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

270

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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Helicobacter pylori and gastric acid: Biological and therapeutic implications

Cited by 204 publications

References 12 publications

Profiling of bacterial flora in gastric biopsies from patients with Helicobacter pylori-associated gastritis and histologically normal control individuals by temperature gradient gel electrophoresis and 16S rDNA sequence analysis

Profiling of bacterial flora in gastric biopsies from patients with Helicobacter pylori-associated gastritis and histologically normal control individuals by temperature gradient gel electrophoresis and 16S rDNA sequence analysis

Identification of Campylobacter jejuni Genes Contributing to Acid Adaptation by Transcriptional Profiling and Genome-Wide Mutagenesis

Epithelial attachment alters the outcome of Helicobacter pylori infection

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