| pubmed-article:19179414 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C0085508 | lld:lifeskim |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C0085424 | lld:lifeskim |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:19179414 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:19179414 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19179414 | pubmed:dateCreated | 2009-3-16 | lld:pubmed |
| pubmed-article:19179414 | pubmed:abstractText | Interleukin-12 (IL-12) is a heterodimeric cytokine produced by antigen-presenting cells that promotes the development of T-helper lymphocyte 1 (Th1). Chronic gastritis induced by Helicobacter pylori is considered a Th1-mediated process. IL-12 levels in gastric biopsy samples of H. pylori-infected patients are higher than in those of uninfected individuals, but the cellular source of IL-12 remains elusive. IL-12 staining was detected in mucosal epithelial cells, lymphocytes, and macrophages in specimens of patients with H. pylori-positive gastritis. Therefore, we investigated IL-12 p40 mRNA induction by H. pylori in gastric epithelial cells and T cells. Although cag pathogenicity island (PAI)-positive H. pylori induced IL-12 p40 mRNA expression, an isogenic mutant of the cag PAI failed to induce it in both cell types. Supernatants from H. pylori cultures and H. pylori VacA induced IL-12 p40 mRNA expression in T cells but not in epithelial cells. The activation of the IL-12 p40 promoter by H. pylori was mediated through NF-kappaB. The transfection of IkappaB kinase and NF-kappaB-inducing kinase dominant-negative mutants inhibited H. pylori-induced IL-12 p40 activation. Inhibitors of NF-kappaB, phosphatidylinositol 3-kinase, p38 mitogen-activated protein kinase, and Hsp90 suppressed H. pylori- and VacA-induced IL-12 p40 mRNA expression. The results indicate that H. pylori induces IL-12 p40 expression by the activation of NF-kappaB, phosphatidylinositol 3-kinase, and p38 mitogen-activated protein kinase. Hsp90 is also a crucial regulator of H. pylori-induced IL-12 p40 expression. In addition to the cag PAI, VacA might be relevant in the induction of IL-12 expression and a Th1-polarized response only in T cells. | lld:pubmed |
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| pubmed-article:19179414 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19179414 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19179414 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19179414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19179414 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19179414 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19179414 | pubmed:issn | 1098-5522 | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:FujitaJiroJ | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:MoriNaokiN | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:SenbaMasachik... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:SasakawaChihi... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:HirayamaToshi... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:MimuroHitomiH | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:KinjoFukunori... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:D'AmbrosioDan... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:TomimoriKohK | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:IshikawaChieC | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:TeruyaHiromit... | lld:pubmed |
| pubmed-article:19179414 | pubmed:author | pubmed-author:TakeshimaErik... | lld:pubmed |
| pubmed-article:19179414 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19179414 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:19179414 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19179414 | pubmed:authorsComplete | Y | lld:pubmed |
