Mechanism of cag pathogenicity island-positive Helicobacter pylori mediated inflammatory reaction
| Project/Area Number |
16590364
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Nagasaki University |
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Principal Investigator |
WADA Akihiro Nagasaki University, Institute of Tropical Medicine, Lecturer, 熱帯医学研究所, 講師 (70253698)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | H.pylori / NF-κB / CagA / Nod1 / Cag / 炎症 |
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| Research Abstract |
The unknown factor of cag pathogenicity island (PAI)-positive Helicobacter pylori can induce activation of NF-κB in mammalian cells. NF-κB activation is very important for inflammatory reaction in gastric cells. In order to determine the activity of cag PAI-dependent NF-κB activation factor in host cells, we employed assay system to examined the purified unknown factor. However, Viala et al. reported that peptidoglycan was delivered to host cells by a bacterial type IV secretion system, encoded by the H.pylori cag PAI whereby NF-κB activation is induced via Nod1 (Nat.Immunol., 2004).
We examined the signal transduction of NF-κB activation by injecting peptidoglycan via Nod1 in host cells in detail. Although cag PAI-positive H.pylori induced NF-κB activation in MKN45 cells, H.pylori could not activate NF-κB in AZ-521 cells. To better understand this cell-type specific results of NF-κB activation, Nod1 mRNA expression level were examined by RT-PCR. Nod1 is a activator of NF-κB for detecting peptidoglycan. Based on this results, we suggest that Nod1 mRNA expression level could not account for different sensitivity of two cell lines. As accordingly, level of effector injected for a type IV secretion system of H. pylori was examined. CagA is one of effector of H.pylori, and is Tyr-phosphorilated by host Tyr-kinase. Tyr-CagA level in AZ-521 cells is weaker than that in MKN45 cells. These results suggested that type IV secretion system of H.pylori may have cell-type specificity for injection of the effector.
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Report
(3 results)
Research Products
(17 results)
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[Journal Article] Helicobacter pylori vacuolating cytotoxin induces activation of the proapoptotic protein Bax and Bak, leading to cytochrome c release and cell death, independent of vacuolation.2006
Author(s)
Yamasaki E, Wada A, Kumatori A, Nakagawa I, Funao J, Nakayama M, Hisatsune J, Kimura M, Moss J, Hirayama T
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Journal Title
Description
「研究成果報告書概要(欧文)」より
Related Report
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[Journal Article] Cytotoxicity and recognition of receptor-like protein tyrosine phosphatases, RPTPalpha and RPTPbeta, by Helicobacter pylori m2VacA.2005
Author(s)
De Guzman BB, Hisatsune J, Nakayama M, Yahiro K, Wada A, Yamasaki E, Nishi Y, Yamazaki S, Azuma T, Ito Y, Ohtani M, van der Wijk T, den Hertog J, Moss J, Hirayama T.
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Journal Title
Cell Microbiol. 7(9)
Pages: 1285-1293
Description
「研究成果報告書概要(欧文)」より
Related Report
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[Journal Article] Functional antagonism between Helicobacter pylori CagA and vacuolating toxin VacA in control of the NFAT signaling pathway in gastric epithelial cells.2005
Author(s)
Yokoyama K, Higashi H, Ishikawa S, Fujii Y, Kondo S, Kato H, Azuma T, Wada A, Hirayama T, Aburatani H, Hatakeyama M.
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Journal Title
Proc Natl Acad Sci U S A. 102(27)
Pages: 9661-9666
Description
「研究成果報告書概要(欧文)」より
Related Report
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