| Project/Area Number |
07670002
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | YAMAGATA UNIVERSITY |
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Principal Investigator |
SASAKI Katsunori YAMAGATA UNIVERSITY,SCHOOL OF MEDICINE,ASSOCIATE PROFESSOR, 医学部, 助教授 (30170666)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | PERITONEUM / PERITONITIS / CELLULAR ADHESION MOLECULES / immunoSEM |
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| Research Abstract |
To establish the peritoneum as defense organ, interaction between the peritoneal mesothelial cells and immuneassociated cells were analyzed morphologically through expression of cellular adhesion molecules with immunoSEM.ICAM-1 (intercellular adhesion molecule-1) is an important molecule of IgG superfamily associated with leukocyte migration through stick adhesion. This molecule was selectively expressed on the microvilli of the peritoneum and was upregulated by LPS (Lipopolysaccharide). The peak was 24 hrs after stimulation. ICAM-1 was suggested to work in both normal and inflammatory conditions.
In the experimental peritonitis, a large number of macrophages appeared on the peritoneum. They had LFA-1 (leukocyte function-associated antigen 1) and Mac-1, which are ligands of ICAM-1, on the cell surface. Mac-1 was restricted to the microvilli of the macrophages in activated condition. The microvilli of the peritoneum expressed ICAM-1 moderately. It was confirmed that these abhesions was necessary for iinteraction between the peritoneum and leukocytes.
The peritoneum expressed VCAM-1 in addition to ICAM-1 after LPS stimulation. Other adhesions (ICAM-2, ELAM-1, PECAM-1, CD105) were not detected. VCAM-1 was restricted to microvilli as well as ICAM-1. After both expression, s leukocytes fixed to the peritoneum Double immunostaining showed localizations of ICAM-1 and VCAM-1 were near to each other.
These results showed that (1) Microvilli with ICAM-1 is a road for leukocyte migration in the normal condition and (2) in inflammation, ICAM-1 and VCAM-1 cooperate to fix leukocytes to the peritoneum and the peritoneum works as defense organ through interaction of ICAM-1 and VCAM-1 with LFA-1, Mac-1 and VLA-4.
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