ArticleInfection and immunity2001
Role of Helicobacter pylori cag region genes in colonization and gastritis in two animal models.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Article
- TLR9 activation suppresses inflammation in response to Helicobacter pylori infection.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Helicobacter pylori modulates host cell survival regulation through the serine-threonine kinase, 3-phosphoinositide dependent kinase 1 (PDK-1).BMC microbiology · 2015Article
- Role of energy sensor TlpD of Helicobacter pylori in gerbil colonization and genome analyses after adaptation in the gerbil.Infection and immunity · 2013Article
- Functional plasticity in the type IV secretion system of Helicobacter pylori.PLoS pathogens · 2013Article
- Suppression of IL-8 production in gastric epithelial cells by MUC1 mucin and peroxisome proliferator-associated receptor-γ.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- The Helicobacter pylori autotransporter ImaA (HP0289) modulates the immune response and contributes to host colonization.Infection and immunity · 2012Article
- Cell-associated hemolysis induced by Helicobacter pylori is mediated by phospholipases with mitogen-activated protein kinase-activating properties.Journal of clinical microbiology · 2012Article
- Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Helicobacter pylori exploits cholesterol-rich microdomains for induction of NF-kappaB-dependent responses and peptidoglycan delivery in epithelial cells.Infection and immunity · 2010Article
- Muc1 cell surface mucin attenuates epithelial inflammation in response to a common mucosal pathogen.The Journal of biological chemistry · 2010Article
- Helicobacter pylori in dental plaque and stomach of patients from Northern Brazil.World journal of gastroenterology · 2010Article
- The cag PAI is intact and functional but HP0521 varies significantly in Helicobacter pylori isolates from Malaysia and Singapore.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010Article
- Helicobacter hepaticus HHGI1 is a pathogenicity island associated with typhlocolitis in B6.129-IL10 tm1Cgn mice.Microbes and infection · 2008Article
- Molecular characterization of Helicobacter pylori VacA induction of IL-8 in U937 cells reveals a prominent role for p38MAPK in activating transcription factor-2, cAMP response element binding protein, and NF-kappaB activation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Helicobacter pylori induces an antimicrobial response in rhesus macaques in a cag pathogenicity island-dependent manner.Gastroenterology · 2008Article
- NF-kappaB activation during acute Helicobacter pylori infection in mice.Infection and immunity · 2008Article
- Helicobacter pylori chemotaxis modulates inflammation and bacterium-gastric epithelium interactions in infected mice.Infection and immunity · 2007Article
- Helicobacter pylori-secreting protein Tipalpha is a potent inducer of chemokine gene expressions in stomach cancer cells.Journal of cancer research and clinical oncology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The Helicobacter pylori chromosomal region known as the cytotoxin-gene associated pathogenicity island (cag PAI) is associated with severe disease and encodes proteins that are believed to induce interleukin (IL-8) secretion by cultured epithelial cells. The objective of this study was to evaluate the relationship between the cag PAI, induction of IL-8, and induction of neutrophilic gastric inflammation. Germ-free neonatal piglets and conventional C57BL/6 mice were given wild-type or cag deficient mutant derivatives of H. pylori strain 26695 or SS1. Bacterial colonization was determined by plate count, gastritis and neutrophilic inflammation were quantified, and IL-8 induction in AGS cells was determined by enzyme-linked immunosorbent assay. Deletion of the entire cag region or interruption of the virB10 or virB11 homolog had no effect on bacterial colonization, gastritis, or neutrophilic inflammation. In contrast, these mutations had variable effects on IL-8 induction, depending on the H. pylori strain. In the piglet-adapated strain 26695, which induced IL-8 secretion by AGS cells, deletion of the cag PAI decreased induction. In the mouse-adapted strain SS1, which did not induce IL-8 secretion, deletion of the cagII region or interruption of any of three cag region genes increased IL-8 induction. These results indicate that in mice and piglets (i) neither the cag PAI nor the ability to induce IL-8 in vitro is essential for colonization or neutrophilic inflammation and (ii) there is no direct relationship between the presence of the cag PAI, IL-8 induction, and neutrophilic gastritis.
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