ArticleThe Journal of biological chemistry2008
Regulation of the Helicobacter pylori cellular receptor decay-accelerating factor.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 21 citations in OpenAlex.
- The active form of Helicobacter pylori vacuolating cytotoxin induces decay-accelerating factor CD55 in association with intestinal metaplasia in the human gastric mucosa.The Journal of pathology · 2022Article
- H. pylori infection induced BMAL1 expression and rhythm disorder aggravate gastric inflammation.EBioMedicine · 2019Article
- Helicobacter pylori-induced miR-135b-5p promotes cisplatin resistance in gastric cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Blood Groups in Infection and Host Susceptibility.Clinical microbiology reviews · 2015Review
- Malaria. A forward genetic screen identifies erythrocyte CD55 as essential for Plasmodium falciparum invasion.Science (New York, N.Y.) · 2015Article
- Pathogenesis of human diffusely adhering Escherichia coli expressing Afa/Dr adhesins (Afa/Dr DAEC): current insights and future challenges.Clinical microbiology reviews · 2014Review
- PI3K/Akt pathway restricts epithelial adhesion of Dr + Escherichia coli by down-regulating the expression of decay accelerating factor.Experimental biology and medicine (Maywood, N.J.) · 2014Article
- Complement protective epitopes and CD55-microtubule complexes facilitate the invasion and intracellular persistence of uropathogenic Escherichia coli.The Journal of infectious diseases · 2014Article
- Helicobacter pylori promotes the expression of Krüppel-like factor 5, a mediator of carcinogenesis, in vitro and in vivo.PloS one · 2013Article
- Sex-specific signaling through Toll-Like Receptors 2 and 4 contributes to survival outcome of Coxsackievirus B3 infection in C57Bl/6 mice.Biology of sex differences · 2012Article
- Cell-associated hemolysis induced by Helicobacter pylori is mediated by phospholipases with mitogen-activated protein kinase-activating properties.Journal of clinical microbiology · 2012Article
- Helicobacter pylori induction of eosinophil migration is mediated by the cag pathogenicity island via microbial-epithelial interactions.The American journal of pathology · 2011Article
- Helicobacter infection alters MyD88 and Trif signalling in response to intestinal ischaemia-reperfusion.Experimental physiology · 2011Article
- Hemorrhage-induced intestinal damage is complement-independent in Helicobacter hepaticus-infected mice.Shock (Augusta, Ga.) · 2010Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for peptic ulceration and distal gastric cancer, and adherence of H. pylori to gastric epithelial cells is critical for induction of inflammation. One H. pylori constituent that increases disease risk is the cag pathogenicity island, which encodes a secretion system that translocates bacterial effector molecules into host cells. Decay-accelerating factor (DAF) is a cellular receptor for H. pylori and a mediator of the inflammatory response to this pathogen. H. pylori induces DAF expression in human gastric epithelial cells; therefore, we sought to define the mechanism by which H. pylori up-regulates DAF and to extend these findings into a murine model of H. pylori-induced injury. Co-culture of MKN28 gastric epithelial cells with the wild-type H. pylori cag(+) strain J166 induced transcriptional expression of DAF, which was attenuated by disruption of a structural component of the cag secretion system (cagE). H. pylori-induced expression of DAF was dependent upon activation of the p38 mitogen-activated protein kinase pathway but not NF-kappaB. Hypergastrinemic INS-GAS mice infected with wild-type H. pylori demonstrated significantly increased DAF expression in gastric epithelium versus uninfected controls or mice infected with an H. pylori cagE(-) isogenic mutant strain. These results indicate that H. pylori cag(+) strains induce up-regulation of a cognate cellular receptor in vitro and in vivo in a cag-dependent manner, representing the first evidence of regulation of an H. pylori host receptor by the cag pathogenicity island.
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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.