Source:http://linkedlifedata.com/resource/pubmed/id/20038537
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-2-19
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pubmed:abstractText |
Colonization of the gastric mucosa by Helicobacter pylori can lead to serious clinical outcomes, including gastric cancer. Toll-like receptors (TLRs) play an important role in the host response to H. pylori through the recognition of pathogen-associated molecular patterns. TLR9, in particular, is partly responsible for initiating bacterial induced immunity by binding unmethylated CpG-DNA, which is abundant in bacteria. A well-documented single nucleotide polymorphism (SNP) within the TLR9 promoter (TLR9 -1237T/C), is associated with a variety of inflammatory disorders, including allergic asthma, inflammatory bowel disease, and atopy. Analysis of the TLR9 promoter gene sequence has shown that carriage of the variant "C" allele at position -1237 creates a potential NF-kappaB binding site that would theoretically increase the transcriptional activity of the gene. In this study, we report that the TLR9 -1237 C allele was significantly associated with the development of H. pylori-induced premalignant gastric changes. Functional analysis of the SNP, supporting the data generated from the genetic association study, showed that carriage of the C allele increased TLR9 transcriptional activity driven mainly by activation of NF-kappaB. Collectively, these findings confirm that the TLR9 -1237T/C polymorphism is a risk factor for the development of H. pylori-induced premalignant gastric changes and provide a plausible mechanistic explanation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1098-5522
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pubmed:author |
pubmed-author:BerrySusanS,
pubmed-author:CrockettJulie CJC,
pubmed-author:El-OmarEmad MEM,
pubmed-author:HoldGeorgina LGL,
pubmed-author:HopeMairi EME,
pubmed-author:McCollKenneth E LKE,
pubmed-author:McLeanMairi HMH,
pubmed-author:NgMike Tsz HinMT,
pubmed-author:ThomsonJohnJ,
pubmed-author:Van't HofRobR
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pubmed:issnType |
Electronic
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1345-52
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pubmed:dateRevised |
2010-9-2
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pubmed:meshHeading |
pubmed-meshheading:20038537-Gene Expression,
pubmed-meshheading:20038537-Gene Frequency,
pubmed-meshheading:20038537-Helicobacter Infections,
pubmed-meshheading:20038537-Helicobacter pylori,
pubmed-meshheading:20038537-Humans,
pubmed-meshheading:20038537-NF-kappa B,
pubmed-meshheading:20038537-Polymorphism, Single Nucleotide,
pubmed-meshheading:20038537-Promoter Regions, Genetic,
pubmed-meshheading:20038537-Protein Binding,
pubmed-meshheading:20038537-Scotland,
pubmed-meshheading:20038537-Toll-Like Receptor 9,
pubmed-meshheading:20038537-Up-Regulation
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pubmed:year |
2010
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pubmed:articleTitle |
Increase in NF-kappaB binding affinity of the variant C allele of the toll-like receptor 9 -1237T/C polymorphism is associated with Helicobacter pylori-induced gastric disease.
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pubmed:affiliation |
Division of Applied Medicine, Aberdeen University, Aberdeen AB25 2ZD, Scotland, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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