1995 Fiscal Year Final Research Report Summary
Study on defense mechanism of the placenta and fetus against HTLV-I transmission from mother to fetus
| Project/Area Number |
05671383
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kagoshima University |
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Principal Investigator |
FUJINO Toshinori Kagoshima University, School of Allied Medical Sciences, Associate Professor, 医療技術短期大学部, 助教授 (90165407)
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| Co-Investigator(Kenkyū-buntansha) |
YASHIKI Shinji Kagoshima University, Faculty of Medicine, Department of Virology, Research Asso, 医学部, 助手 (40182315)
NAGATA Yukihiro Kagoshima University, Faculty of Medicine, Department of Obstetrics and Gynecolo, 医学部, 教授 (30038806)
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| Project Period (FY) |
1993 – 1995
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| Keywords | HTLV-I / Intrauterine infection / Defense mechanism / Placenta / Fetus / Apoptosis |
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| Research Abstract |
This study was done to investigate defense mechanisms of the placenta and fetus against human T-lymphotropic virus type I (HTLV-I) transmission from mother to fetus.
Placentas and cord blood lymphocytes (CBL) were tested for HTLV-I infection.
Apoptosis in the placentas was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling method. CD8, CD14, CD68-positive cells in the placentas were tested by immunohistochemistry. Co-cultivation of placental villous cells with an HTLV-I-infected cell line was performed. Epstein-Barr virus (EBV) transformation was performed in CBL.
Eight of 16 (50%) placentas from HTLV-I-seropositive mothers were infected with HTLV-I.None of the CBL were infected. The incidence of apoptosis-positive cells in the HTLV-I-infected placentas was higher than those of HTLV-I-seronegative (p<0.05). CD8^+cells, CD14^+cells, and CD68^+cells were detected in the placentas. Placental macrophage-like cells had the capacity to phagocytose the HTLV-I-infected cells. Production of antibodies against HTLV-I was inducible by EBV transformation of CBL.
It was suggested that the placenta served as a barrier to HTLV-I transmission from mother to fetus through an apoptosis-related defense mechanism, and that fetus itself had the capacity to protect HTLV-I infection, where HTLV-I-infection reached to fetal circulation.
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Research Products
(8 results)
