Project/Area Number |
09671702
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Kagoshima University |
Principal Investigator |
FUJINO Toshinori Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (90165407)
|
Co-Investigator(Kenkyū-buntansha) |
NAGATA Yukihiro Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (30038806)
|
Project Period (FY) |
1997 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
|
Keywords | HTLV-I / Intrauterine infection / placenta / Apoptosis / Defense mechanism against infection / 母児感染 / 胎内感染 / バリア機構 |
Research Abstract |
It has been well known that the placenta has a protective action against viral transmission from mother to fetus, which is called "the placental barrier". However, the mechanism of "the placental barrier'' is still not well elucidated. Human T-lymphotropic virus type I (HTLV-I) infection of pregnant women is rarely transmitted to fetuses. In the present study, the association between HTLV-I infection and apoptosis of the placental villous cells was investigated. The results obtained were as follows. 1. TdT mediated UTP nick end labeling method revealed that the incidence of apoptosis-positive placental villous cells in placentas from HTLV-I-seropositive pregnant women (n=8) was significantly higher than HTLV-I-seronegative pregnant women (n=8). 2. Apoptosis was induced in placental villous cells by co-culturing with HTLV-I-infected lymphocytes (MT-2 cells). 3. There was no difference in the weight of term placentas between the HTLV-I-seropositive pregnant women (n=69) and HTLV-I-seronegatives (n=300). The birth weight of the babies showed no difference between the two groups either. 4. Apoptosis was induced in HTLV-I-infected lymphocytes (MT-2 cells), when co-cultured with placenetal villous cells.
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