ReviewFrontiers in cellular and infection microbiology2012
Alterations in Helicobacter pylori triggered by contact with gastric epithelial cells.
Review in Frontiers in cellular and infection microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
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- Outer inflammatory protein a (OipA) of Helicobacter pylori is regulated by host cell contact and mediates CagA translocation and interleukin-8 response only in the presence of a functional cag pathogenicity island type IV secretion system.Pathogens and disease · 2017Article
- The Helicobacter pylori Autotransporter ImaA Tempers the Bacterium's Interaction with α5β1 Integrin.Infection and immunity · 2017Article
- KCTD5 and Ubiquitin Proteasome Signaling Are Required forFrontiers in cellular and infection microbiology · 2017Article
- Coordination of Candida albicans Invasion and Infection Functions by Phosphoglycerol Phosphatase Rhr2.Pathogens (Basel, Switzerland) · 2015Article
- High resolution electron microscopy of the Helicobacter pylori Cag type IV secretion system pili produced in varying conditions of iron availability.Journal of visualized experiments : JoVE · 2014Article
- The host protein calprotectin modulates the Helicobacter pylori cag type IV secretion system via zinc sequestration.PLoS pathogens · 2014Article
- Genes required for assembly of pili associated with the Helicobacter pylori cag type IV secretion system.Infection and immunity · 2014Article
- In depth analysis of the Helicobacter pylori cag pathogenicity island transcriptional responses.PloS one · 2014Article
- Rapid interaction of Helicobacter pylori with microvilli of the polar human gastric epithelial cell line NCI-N87.Anatomical record (Hoboken, N.J. : 2007) · 2013Article
- Research advances in the study of Campylobacter, Helicobacter, and related organisms.Frontiers in cellular and infection microbiology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Helicobacter pylori lives within the mucus layer of the human stomach, in close proximity to gastric epithelial cells. While a great deal is known about the effects of H. pylori on human cells and the specific bacterial products that mediate these effects, relatively little work has been done to investigate alterations in H. pylori that may be triggered by bacterial contact with human cells. In this review, we discuss the spectrum of changes in bacterial physiology and morphology that occur when H. pylori is in contact with gastric epithelial cells. Several studies have reported that cell contact causes alterations in H. pylori gene transcription. In addition, H. pylori contact with gastric epithelial cells promotes the formation of pilus-like structures at the bacteria-host cell interface. The formation of these structures requires multiple genes in the cag pathogenicity island, and these structures are proposed to have an important role in the type IV secretion system-dependent process through which CagA enters host cells. Finally, H. pylori contact with epithelial cells can promote bacterial replication and the formation of microcolonies, phenomena that are facilitated by the acquisition of iron and other nutrients from infected cells. In summary, the gastric epithelial cell surface represents an important niche for H. pylori, and upon entry into this niche, the bacteria alter their behavior in a manner that optimizes bacterial proliferation and persistent colonization of the host.
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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.