Linked Life Data

20007577

Source:http://linkedlifedata.com/resource/pubmed/id/20007577

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-12-16
pubmed:abstractText
Helicobacter pylori rapidly activates MAPKs and transcription factors, NF-kappaB and AP-1, in gastric epithelial cells following host attachment. Activation of these signal transducers is largely dependent on the cag pathogenicity island (cagPAI)-encoded Type IV Secretion System. H. pylori was shown to translocate peptidoglycan through the Type IV Secretion System, which is recognized by the pathogen recognition molecule, NOD1, thus resulting in NF-kappaB activation. The mechanisms of H. pylori-induced MAPK and AP-1 activation, however, are less well defined and therefore, we assessed the contribution of NOD1 to their activation. For this, we used gastric epithelial cell lines, stably expressing siRNA to either NOD1 or a control gene. In siNOD1-expressing cells stimulated with cagPAI(+) H. pylori, we observed significant reductions in p38 and ERK phosphorylation (p < 0.05), whereas the levels of Jnk phosphorylation remained unchanged. Consistent with a previous report, however, we were able to demonstrate NOD1-dependent Jnk phosphorylation by the invasive pathogen Shigella flexneri, highlighting pathogen-specific host responses to infection. We also show that NOD1 was essential for H. pylori induction of not only NF-kappaB, but also AP-1 activation, implying that NOD1 induces robust proinflammatory responses, in an attempt to rapidly control infection. Pharmacological inhibition of p38 and ERK activity significantly reduced IL-8 production in response to H. pylori, further emphasizing the importance of MAPKs in innate immune responses to the pathogen. Thus, for the first time we have shown the important role for NOD1 in MAPK and AP-1 activation in response to cagPAI(+) H. pylori.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8099-109
pubmed:meshHeading
pubmed-meshheading:20007577-Antigens, Bacterial, pubmed-meshheading:20007577-Bacterial Outer Membrane Proteins, pubmed-meshheading:20007577-Bacterial Proteins, pubmed-meshheading:20007577-Cell Line, pubmed-meshheading:20007577-Cell Line, Tumor, pubmed-meshheading:20007577-Enzyme Activation, pubmed-meshheading:20007577-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:20007577-Gene Targeting, pubmed-meshheading:20007577-Helicobacter pylori, pubmed-meshheading:20007577-Humans, pubmed-meshheading:20007577-Inflammation Mediators, pubmed-meshheading:20007577-MAP Kinase Kinase 4, pubmed-meshheading:20007577-Nod1 Signaling Adaptor Protein, pubmed-meshheading:20007577-Phosphorylation, pubmed-meshheading:20007577-Secretory Vesicles, pubmed-meshheading:20007577-Signal Transduction, pubmed-meshheading:20007577-Transcription Factor AP-1
pubmed:year
2009
pubmed:articleTitle
Helicobacter pylori induces MAPK phosphorylation and AP-1 activation via a NOD1-dependent mechanism.
pubmed:affiliation
Department of Microbiology, Monash University, Clayton, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't