ArticleInfection and immunity2005
Helicobacter pylori activates myosin light-chain kinase to disrupt claudin-4 and claudin-5 and increase epithelial permeability.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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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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
54 citing papers in PubMed, 125 citations in OpenAlex.
- Long term platelet responses to Helicobacter pylori eradication in Canadian patients with immune thrombocytopenic purpura.International journal of hematology · 2008Trial
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- Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens.PLoS pathogens · 2025Review
- Article
- The role of gut microbiota augmentation in managing non-alcoholic fatty liver disease: an in-depth umbrella review of meta-analyses with grade assessment.Annals of medicine and surgery (2012) · 2024Review
- Both extracellular vesicles from helicobacter pylori-infected cells and helicobacter pylori outer membrane vesicles are involved in gastric/extragastric diseases.European journal of medical research · 2023Review
- Helicobacter pylori outer membrane vesicles induce astrocyte reactivity through nuclear factor-κappa B activation and cause neuronal damage in vivo in a murine model.Journal of neuroinflammation · 2023Article
- Leaky Gut and the Ingredients That Help Treat It: A Review.Molecules (Basel, Switzerland) · 2023Review
- Gastric precancerous lesions:occurrence, development factors, and treatment.Frontiers in oncology · 2023Review
- Is Helicobacter pylori infection associated with non-alcoholic fatty liver disease in individuals undergoing bariatric surgery? Cross-sectional study.Sao Paulo medical journal = Revista paulista de medicina · 2023Observational
- Helicobacter pylori infection in the stomach induces neuroinflammation: the potential roles of bacterial outer membrane vesicles in an animal model of Alzheimer's disease.Inflammation and regeneration · 2022Review
- The immune microenvironment in gastric adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2022Review
- Article
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Tight Junctions as a Key for Pathogens Invasion in Intestinal Epithelial Cells.International journal of molecular sciences · 2021Review
- Role ofClinical, cosmetic and investigational dermatology · 2021Article
- Protein losing gastroenteropathy due toBMJ case reports · 2019Article
- Impact of microbiota in colorectal carcinogenesis: lessons from experimental models.Intestinal research · 2018Review
- Afadin Downregulation byFrontiers in microbiology · 2018Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a spiral, gram-negative bacterium that specifically and persistently infects the human stomach. In some individuals, H. pylori-induced chronic gastritis may progress to gastroduodenal ulcers and gastric cancer. Currently, the host-microbe interactions that determine the clinical outcome of infection are not well defined. H. pylori strains capable of disrupting the gastric epithelial barrier may increase the likelihood of developing serious disease. In this study, H. pylori strain SS1 increased gastric, but not small intestinal, permeability in C57BL/6 mice. H. pylori strain SS1 was able to directly increase paracellular permeability, in the absence of host inflammatory cells, by disrupting the tight-junctional proteins occludin, claudin-4, and claudin-5 in confluent nontransformed epithelial cells. H. pylori SS1 also reduced claudin-4 protein levels in human gastric AGS cells. The ability of H. pylori SS1 to increase permeability appeared to be independent of the well-characterized virulence factors vacuolating cytotoxin and CagA protein. H. pylori activated myosin light-chain kinase in epithelial cells to phosphorylate myosin light chain and increase permeability by disrupting claudin-4 and claudin-5. The bacterial factor responsible for increasing epithelial permeability was heat sensitive, membrane bound, and required apical contact with monolayers. In conclusion, disruptions of the tight junctions observed in this study implicate host cell signaling pathways, including the phosphorylation of myosin light chain and the regulation of tight-junctional proteins claudin-4 and claudin-5, in the pathogenesis of H. pylori infection.
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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.