2003 Fiscal Year Final Research Report Summary
Host-response in gastric mucosa in fected with Helicobacter pylori
| Project/Area Number |
14571187
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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 |
Digestive surgery
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| Research Institution | Shinshu University Hospital |
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Principal Investigator |
SUGIYAMA Atsushi Shinshu University Hospital, Associate Professor, 医学部附属病院, 助教授 (90187675)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Helicobacter pylori / gastric cancer / chronic gastritis / Duodenogastric reflux / Mongolian gerbil / prostaglandine / Cytokine / プロスタグランディン |
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| Research Abstract |
Our experiments revealed the followings :
1.The animal model of duodeno-gastric reflux (DGR) was established using Mongolian gerbils (MGs). The DGR accelerated the turnover of gastric epithelial cells, although it decreased the activity of HP-induced gastritis in the early phase of the gastritis. The alterations of bacterial flora in stomach caused the DGR.
2.a4GnT is a key-enzyme to regulate the production of glandular mucous mucin. mRNA-expression of a4GnT, IL-1B, TNFa, IL-4,IL 6 and IL-10 were quantified at some points after inoculation of HP in MGs. Results : (1)mRNA-expression of a4GnT increased at early phase of HP-induced gastritis. (2)IL-1B and TNFa showed same response as a4GnT. (3)IL-4,6 and 10 increased at the late phase of HP-induced gastritis. Immune response of the gastric mucosa changed with time from Th1-to Th2-dominant. (4)Thick mucoid-caps of glandular mucous mucin were formed at mucosal surface of the stomach infected with HP.
3.The extract essence of rice inhibits HP-induced gastritis.
4.The expression of cytokines (both Th1 and Th2) increased in MGs that were treated with HP and nitroso-compounds. MG is a useful animal model to investigate the relationship among HP-infection, host-response and environmental factors.
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