ArticleInfection and immunity2013
Helicobacter pylori-induced disruption of monolayer permeability and proinflammatory cytokine secretion in polarized human gastric epithelial cells.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Effects of extensive protein hydrolysate in supporting intestinal barrier function in vitro.Pediatric research · 2026Article
- Development of a novel organoid-based two-dimensional system to model the intestinal host-parasite interface in fasciolosis.Frontiers in cellular and infection microbiology · 2026Article
- Antibiotics Impact the Cytotoxicity and Cytopathic Effect ofInternational journal of molecular sciences · 2025Article
- Article
- Novel Bacteroides Vulgatus strain protects against gluten-induced break of human celiac gut epithelial homeostasis: a pre-clinical proof-of-concept study.Pediatric research · 2024Article
- A foundational approach to culture and analyze malnourished organoids.Gut microbes · 2023Article
- Accumulation of Deleterious Effects in Gastric Epithelial Cells and Vascular Endothelial Cells In Vitro in the Milieu ofInternational journal of molecular sciences · 2022Article
- Review
- Interference of LPSCells · 2021Article
- Article
- Tight Junctions as a Key for Pathogens Invasion in Intestinal Epithelial Cells.International journal of molecular sciences · 2021Review
- Parkinson's disease: Are gut microbes involved?American journal of physiology. Gastrointestinal and liver physiology · 2020Review
- Expression of Tight Junction Proteins According to Functional Dyspepsia Subtype and Sex.Journal of neurogastroenterology and motility · 2020Article
- Review
- Changes of tight junction and interleukin-8 expression using a human gastroid monolayer model of Helicobacter pylori infection.Helicobacter · 2019Article
- Human gut derived-organoids provide model to study gluten response and effects of microbiota-derived molecules in celiac disease.Scientific reports · 2019Article
- Acidic bile salts induces mucosal barrier dysfunction throughOncotarget · 2018Article
- Modulation of Intestinal Paracellular Transport by Bacterial Pathogens.Comprehensive Physiology · 2018Review
- Afadin Downregulation byFrontiers in microbiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Helicobacter pylori infection of the stomach is related to the development of diverse gastric pathologies. The ability of H. pylori to compromise epithelial junctional complexes and to induce proinflammatory cytokines is believed to contribute to pathogenesis. The purpose of this study was to use an in vitro human gastric epithelial model to investigate the ability of H. pylori to affect permeability and the extent and polarity of the host inflammatory response. NCI-N87 monolayers were cocultured with live or heat-killed H. pylori or culture supernatants. Epithelial barrier function was measured by transepithelial electric resistance (TEER) analysis, diffusion of fluorescein isothiocyanate (FITC)-labeled markers, and immunostaining for tight junction proteins. Supernatants from both apical and basolateral chambers were tested for cytokine production by multiplex analysis. H. pylori caused a significant decrease in TEER, an increased passage of markers through the infected monolayer, and severe disruption and mislocalization of ZO-1 and claudin-1 proteins. Cell viability was not altered by H. pylori, indicating that loss of barrier function could be attributed to a breakdown of tight junction integrity. Significantly high levels of cytokine secretion were induced by either viable or heat-killed H. pylori. H. pylori affects monolayer permeability of polarized human gastric epithelial cells. Proinflammatory cytokines were secreted in a polarized manner, mostly basolaterally. Live bacteria are required for disruption of tight junctions but not for the induction of cytokine secretion. The NCI-N87 cell line provides an excellent model for the in vitro study of H. pylori pathogenesis and the epithelial cell host response to infection.
Indexed as
Identifiers
What OpenQuestion holds
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.