ArticleInfection and immunity2002
Specific entry of Helicobacter pylori into cultured gastric epithelial cells via a zipper-like mechanism.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 157 citations in OpenAlex.
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- Time-Resolved Transcriptional Profiling of Epithelial Cells Infected by IntracellularMicroorganisms · 2021Article
- Clinical Strains ofFrontiers in pharmacology · 2021Article
- Metabolic Glycan Labeling-Based Screen to Identify Bacterial Glycosylation Genes.ACS infectious diseases · 2020Article
- Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells.BMC cancer · 2020Article
- Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate.Seminars in cell & developmental biology · 2020Review
- Type IV secretion ofGut pathogens · 2020Article
- T4SS-dependent TLR5 activation by Helicobacter pylori infection.Nature communications · 2019Article
- Establishment of serine protease htrA mutants in Helicobacter pylori is associated with secA mutations.Scientific reports · 2019Article
- Nonhelical Helicobacter pylori Mutants Show Altered Gland Colonization and Elicit Less Gastric Pathology than Helical Bacteria during Chronic Infection.Infection and immunity · 2019Article
- Current and Future Treatment of Helicobacter pylori Infections.Advances in experimental medicine and biology · 2019Review
- Pathway Interactions Based on Drug-Induced Datasets.Cancer informatics · 2019Article
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- Phosphatidylinositol-(3,4,5)-Trisphosphate Induces Phagocytosis of Nonmotile Pseudomonas aeruginosa.Infection and immunity · 2018Article
- Unusual Manifestation of LiveInternational journal of molecular sciences · 2018Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although Helicobacter pylori has generally been considered an extracellular pathogen, a number of in vitro infection experiments and biopsy examinations have shown that it is capable of occasionally entering mammalian host cells. Here, we characterized this entry process by using AGS cells as a host cell model. In gentamicin protection-invasion assays, the number of H. pylori colonies recovered was lower than that for Salmonella enterica serovar Typhimurium X22, Escherichia coli expressing InvA, and Yersinia enterocolitica YO:9 grown at 25 degrees C but higher than that for Neisseria gonorrhoeae VP1 and Y. enterocolitica YO:9 grown at 37 degrees C. At the ultrastructural level, the entry process was observed to occur via a zipper-like mechanism. Internalized H. pylori was bound in tight LAMP-1-containing vacuoles in close association with condensed filamentous actin and tyrosine phosphorylation signals. Wortmannin, a potent inhibitor of phosphatidylinositol 3-kinase, and calphostin C, an inhibitor of protein kinase C, both inhibited the entry of H. pylori in a sensitive and dose-dependent manner; however, the level of entry was enhanced by sodium vanadate, an inhibitor of tyrosine phosphatases and ATPases. Furthermore, the cytokine tumor necrosis factor alpha antagonized the entry of H. pylori into AGS cells. Collectively, these results demonstrate that the entry of H. pylori into AGS cells occurs via a zipper-like mechanism which involves various host signal transduction events.
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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.