Linked Life Data

15628712

Source:http://linkedlifedata.com/resource/pubmed/id/15628712

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11-12
pubmed:dateCreated
2005-1-4
pubmed:abstractText
Helicobacter pylori colonization of the stomach results in a chronic-active gastritis characterized by mucosal infiltration of both neutrophils and lymphocytes. A T helper lymphocyte (Th1) profile predominates, which promotes the chronic and persistent inflammatory changes in the gastric mucosa in response to this bacterial pathogen. The cytokine interleukin-18 induces production of interferon-gamma by activated T lymphocytes and promotes a Th1 profile. An in vitro model system was utilized to determine the role of interleukin-18 in response to infection of gastric epithelial cells by H. pylori. H. pylori isolates, characterized with respect to cagE and cagA and VacA status, were employed to infect AGS gastric epithelial cells. Interleukin-18 production was determined by immunoassay. Infection of AGS cells with H. pylori resulted in a 1.8-fold increase in interleukin-18 compared to uninfected cells (22.7+/-2.4 vs. 12.7+/-2.2 pg/ml; P < 0.005). This interleukin-18 response was independent of the cagE status of infecting strains (23.3+/-1.9 vs. 26.3+/-3.6 pg/ml; P = NS). Exposure of AGS cells to recombinant interleukin-18 resulted in dose-dependent and time-dependent secretion of interleukin-8 that was maximal following exposure to 100 pg/ml interleukin-18 for 24 hr (292+/-5 pg/ml, versus 102+/-14 pg/ml in unstimulated cells; P < 0.001). Interleukin-8 secretion was inhibited following pretreatment of cells with anti-interleukin-18 antibody and by pharmacological inhibition of the nuclear transcription factor, NF-kappaB. These findings demonstrate that interleukin-18 can enhance host chemokine response to H. pylori infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0163-2116
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1830-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Helicobacter pylori infection induces interleukin-18 production in gastric epithelial (AGS) cells.
pubmed:affiliation
Sydney Children's Hospital and School of Women's and Children's Health, University of New South Wales, Sydney, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't