ArticleProceedings of the National Academy of Sciences of the United States of America2003
The impact of parietal cells on Helicobacter pylori tropism and host pathology: an analysis using gnotobiotic normal and transgenic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 58 citations in OpenAlex.
- Internalization ofAnnals of medicine · 2026Review
- Metabolic regulator ERRγ governs gastric stem cell differentiation into acid-secreting parietal cells.Cell stem cell · 2024Article
- Reg3 Proteins as Gut Hormones?Endocrinology · 2019Review
- Helicobacter pylori infection progresses proximally associated with pyloric metaplasia in age-dependent tendency: a cross-sectional study.BMC gastroenterology · 2018Article
- Gastrointestinal malignancy and the microbiome.Gastroenterology · 2014Review
- Role of energy sensor TlpD of Helicobacter pylori in gerbil colonization and genome analyses after adaptation in the gerbil.Infection and immunity · 2013Article
- Chronic Helicobacter pylori infection and DNA-damaged stem cells: a recipe for disaster.Digestive diseases and sciences · 2013Article
- The antimicrobial protein REG3A regulates keratinocyte proliferation and differentiation after skin injury.Immunity · 2012Article
- Current molecular markers for gastric progenitor cells and gastric cancer stem cells.Journal of gastroenterology · 2011Review
- Role of innate immunity in Helicobacter pylori-induced gastric malignancy.Physiological reviews · 2010Review
- Helicobacter pylori: gastric cancer and beyond.Nature reviews. Cancer · 2010Review
- Inhibition of heat shock protein expression by Helicobacter pylori.Microbial pathogenesis · 2009Article
- Helicobacter pylori evolution during progression from chronic atrophic gastritis to gastric cancer and its impact on gastric stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- An integrative approach to characterize disease-specific pathways and their coordination: a case study in cancer.BMC genomics · 2008Article
- Symbiotic bacteria direct expression of an intestinal bactericidal lectin.Science (New York, N.Y.) · 2006Article
- Pathogenesis of Helicobacter pylori infection.Springer seminars in immunopathology · 2005Review
- Intracellular Helicobacter pylori in gastric epithelial progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Gastric transcription profile of Helicobacter pylori infection in the rhesus macaque.Infection and immunity · 2004Article
- The spatial orientation of Helicobacter pylori in the gastric mucus.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- A transgenic mouse model of metastatic carcinoma involving transdifferentiation of a gastric epithelial lineage progenitor to a neuroendocrine phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori infection of the human stomach is common and typically benign, although a subset of hosts develops severe pathology. Infection occurs in an organ with distinct microenvironments characterized by pronounced differences in the composition of acid-producing parietal cells. In this study, we examine determinants of bacterial tropism to various gastric niches by using germ-free normal and transgenic mice with an engineered parietal cell ablation. Mice were colonized for 8 weeks with a clinical isolate (Hp1) that expresses adhesins recognized by epithelial NeuAcalpha2,3Galbeta1,4 glycan receptors. In normal mice, Hp1 has tropism for a parietal cell-deficient niche where sialylated glycans are expressed by a narrow band of pit cells positioned at the boundary between the squamous epithelium (forestomach) and the proximal glandular epithelium. Lymphoid aggregates that develop in this niche, but not elsewhere in the stomach, were analyzed by GeneChip and quantitative RT-PCR studies of laser capture microdissected mucosa and yielded a series of biomarkers indicative of immune cell activation and maturation. Genetic ablation of parietal cells produced a new source of NeuAcalpha2,3Galbeta1,4 glycans in amplified gastric epithelial lineage progenitors, with accompanying expansion of Hp1 within the glandular epithelium. Lymphoid aggregates that develop in this formerly acid-protected epithelium have molecular features similar to those observed at the forestomach/glandular junction. These findings demonstrate the important roles played by parietal cells and glycan receptors in determining the positioning of H. pylori within the gastric ecosystem, and emphasize the need to consider the evolution of pathology within a given host in a niche-specific context.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.