ArticleInfection and immunity2010
Helicobacter pylori exploits cholesterol-rich microdomains for induction of NF-kappaB-dependent responses and peptidoglycan delivery in epithelial cells.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- Trained Immunity and Trained Tolerance: The Case ofInternational journal of molecular sciences · 2024Review
- Extracellular vesicles fromCell cycle (Georgetown, Tex.) · 2024Article
- SalivaryWorld journal of gastroenterology · 2022Article
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- Role of lipid rafts in persistentAnnals of translational medicine · 2022Review
- Immunological Perspective:Mediators of inflammation · 2022Review
- Isolation Method and Characterization of Outer Membranes Vesicles ofFrontiers in microbiology · 2021Article
- Could Periodontal Disease through PeriopathogenJournal of clinical medicine · 2020Review
- Cholesteryl α-D-glucoside 6-acyltransferase enhances the adhesion of Helicobacter pylori to gastric epithelium.Communications biology · 2020Article
- Increased Abundance of Clostridium and Fusobacterium in Gastric Microbiota of Patients with Gastric Cancer in Taiwan.Scientific reports · 2018Article
- Article
- A New Role forFrontiers in microbiology · 2017Article
- AFrontiers in cellular and infection microbiology · 2017Article
- miR146a-mediated targeting of FANCM during inflammation compromises genome integrity.Oncotarget · 2016Article
- Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.Gut microbes · 2016Review
- Statin DecreasesFrontiers in cellular and infection microbiology · 2016Article
- Hijacking and Use of Host Lipids by Intracellular Pathogens.Microbiology spectrum · 2015Review
- Dietary, non-microbial intervention to prevent Helicobacter pylori-associated gastric diseases.Annals of translational medicine · 2015Review
- Helicobacter pylori: Genomic Insight into the Host-Pathogen Interaction.International journal of genomics · 2015Review
- The host protein calprotectin modulates the Helicobacter pylori cag type IV secretion system via zinc sequestration.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with Helicobacter pylori cag pathogenicity island (cagPAI)-positive strains is associated with more destructive tissue damage and an increased risk of severe disease. The cagPAI encodes a type IV secretion system (TFSS) that delivers the bacterial effector molecules CagA and peptidoglycan into the host cell cytoplasm, thereby inducing responses in host cells. It was previously shown that interactions between CagL, present on the TFSS pilus, and host α(5)β(1) integrin molecules were critical for CagA translocation and the induction of cytoskeletal rearrangements in epithelial cells. As the α(5)β(1) integrin is found in cholesterol-rich microdomains (known as lipid rafts), we hypothesized that these domains may also be involved in the induction of proinflammatory responses mediated by NOD1 recognition of H. pylori peptidoglycan. Indeed, not only did methyl-β-cyclodextrin depletion of cholesterol from cultured epithelial cells have a significant effect on the levels of NF-κB and interleukin-8 (IL-8) responses induced by H. pylori bacteria with an intact TFSS (P < 0.05), but it also interfered with TFSS-mediated peptidoglycan delivery to cells. Both of these effects could be restored by cholesterol replenishment of the cells. Furthermore, we demonstrated for the first time the involvement of α(5)β(1) integrin in the induction of proinflammatory responses by H. pylori. Taking the results together, we propose that α(5)β(1) integrin, which is associated with cholesterol-rich microdomains at the host cell surface, is required for NOD1 recognition of peptidoglycan and subsequent induction of NF-κB-dependent responses to H. pylori. These data implicate cholesterol-rich microdomains as a novel platform for TFSS-dependent delivery of bacterial products to cytosolic pathogen recognition molecules.
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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.