1998 Fiscal Year Final Research Report Summary
Helicobacter pylori and its association with gastric cancer
| Project/Area Number |
09670502
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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 |
Gastroenterology
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
TAKEDA Hiroshi Medical Hospital, Hokkaido University, Instructor, 医学部・附属病院, 講師 (60261294)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIHIRA Jun School of Medicine, Hokkaido University, Instructor, 医学部, 講師 (30189302)
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| Project Period (FY) |
1997 – 1998
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| Keywords | MIF / H.pylori / parital cell |
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| Research Abstract |
Macrophage migration inhibitory factor (MIF) is the first discovered lymphokine. it was originally identified by its ability to prevent the migration of macrophages out of capillary tubes. Since then, the expression of MIF activities has been found at a variety of inflammatory loci, suggesting its role in regulating the function of macrophages in host defence. More recent reports showed that MIF may have functions besides in the immune system. For instance, MIF mRNA and protein are expressed in anterior pituitary cells, brain, embryonic eye lens and differentiating epidermal cells, suggesting its pivotal role in the regulation of neuroendocrine system, cell growth and differentiation. Furthermore, it is possible that MIF has a role in the gastric mucosal inflammation caused by Helicobacter pylon (HP) infection and the development of gastric cancer in an inflamed gatric mcosa The aim of this study was to elucidatee the role of MIF in the patliogenesis of gastric diseases associated with
… More
HP infection
First, we examined the distribution of MIF in the gastrointestinal tract. MIF mRNA and protein were strongly expressed in the rat gastric mucoca and to a lesser extent in the oesophagus, small intestine and colon by Northern blot analysis and immunoblotting. By immunohistochemical study, positive MIF staining was confined within the cytoplasm of parietal cells. Chief cells and surface mucous cells were negative for MIF staining. Intraperitoneal injection of rat gastrin I caused a decline of MIF mRNA level. After 6 hours of injection, the level of MIF mRNA returned to the level before injection. These results suggest that MIF may play an important role in parietal cell physiology. In human gastric mucosa infected with HP, MIF was strongly expressed in infiltrating lymphocytes as well as gastric parietal cells. Finally, we examined the bood level of MIF before and after the eradication therapy for HP infection. We found that the serum MIF concentration in patients with HP infection was lower than that of HP negative control subjects, and after successful eradication therapy, MIF concentration raised to the level comparable to that of control subjects. These results suggest that the local inflammatory response to HP may have the profound influence on the immune system. Less
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