ArticleGastroenterology2008
Helicobacter pylori induces an antimicrobial response in rhesus macaques in a cag pathogenicity island-dependent manner.
Article in Gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Systematic review with meta-analysis: association between Helicobacter pylori CagA seropositivity and odds of inflammatory bowel disease.Alimentary pharmacology & therapeutics · 2019Pooled it
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- Glycosylation-related gene expression in HT29-MTX-E12 cells upon infection byWorld journal of gastroenterology · 2017Article
- ROS in gastrointestinal inflammation: Rescue Or Sabotage?British journal of pharmacology · 2017Review
- Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise.Free radical biology & medicine · 2017Review
- Molecular Characterization of the Human Stomach Microbiota in Gastric Cancer Patients.Frontiers in cellular and infection microbiology · 2017Article
- Characterization of the Cag pathogenicity island in Helicobacter pylori from naturally infected rhesus macaques.FEMS microbiology letters · 2016Article
- Species variation and spatial differences in mucin expression from corneal epithelial cells.Experimental eye research · 2016Article
- The Gastric Mucosa from Patients Infected with CagA+ or VacA+ Helicobacter pylori Has a Lower Level of Dual Oxidase-2 Expression than Uninfected or Infected with CagA-/VacA- H. pylori.Digestive diseases and sciences · 2016Article
- The cag-pathogenicity island encoded CncR1 sRNA oppositely modulates Helicobacter pylori motility and adhesion to host cells.Cellular and molecular life sciences : CMLS · 2016Article
- DUOX2 Expression Is Increased in Barrett Esophagus and Cancerous Tissues of Stomach and Colon.Gastroenterology research and practice · 2016Article
- Genetic disorders coupled to ROS deficiency.Redox biology · 2015Review
- Dysbiotic infection in the stomach.World journal of gastroenterology · 2015Review
- When an Intramolecular Disulfide Bridge Governs the Interaction of DUOX2 with Its Partner DUOXA2.Antioxidants & redox signaling · 2015Article
- Evidence of convergent evolution in humans and macaques supports an adaptive role for copy number variation of the β-defensin-2 gene.Genome biology and evolution · 2014Article
- Helicobacter pylori downregulates expression of human β-defensin 1 in the gastric mucosa in a type IV secretion-dependent fashion.Cellular microbiology · 2013Article
- Dual oxidases control release of hydrogen peroxide by the gastric epithelium to prevent Helicobacter felis infection and inflammation in mice.Gastroenterology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsWe used the rhesus macaque model to study the effects of the cag pathogenicity island (cag PAI) on the H pylori host-pathogen interaction.
methodsH pylori-specific pathogen-free (SPF) monkeys were experimentally challenged with wild-type (WT) H pylori strain J166 (J166WT, n = 4) or its cag PAI isogenic knockout (J166Deltacag PAI, n = 4). Animals underwent endoscopy before and 1, 4, 8, and 13 weeks after challenge. Gastric biopsies were collected for quantitative culture, histopathology, and host gene expression analysis.
resultsQuantitative cultures showed that all experimentally challenged animals were infected with J166WT or its isogenic J166Deltacag PAI. Histopathology demonstrated that inflammation and expansion of the lamina propria were attenuated in animals infected with J166Deltacag PAI compared with J166WT. Microarray analysis showed that of the 119 up-regulated genes in the J166WT-infected animals, several encode innate antimicrobial effector proteins, including elafin, siderocalin, DMBT1, DUOX2, and several novel paralogues of human-beta defensin-2. Quantitative RT-PCR confirmed that high-level induction of each of these genes depended on the presence of the cag PAI. Immunohistochemistry confirmed increased human-beta defensin-2 epithelial cell staining in animals challenged with J166WT compared with either J166Deltacag PAI-challenged or uninfected control animals.
conclusionsWe propose that one function of the cag PAI is to induce an antimicrobial host response that may serve to increase the competitive advantage of H pylori in the gastric niche and could even provide a protective benefit to the host.
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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.