| Project/Area Number |
04454279
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
小児科学
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| Research Institution | JICHI MEDICAL SCHOOL |
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Principal Investigator |
MATSUI Akira Jichi Medical School, 医学部, 助教授 (00159146)
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| Co-Investigator(Kenkyū-buntansha) |
ARAKAWA Yoichi M.D., 医学部, 講師 (00175184)
SASAKI Nobuhiko MD., 医学部, 講師 (40225884)
TANAKA Toshinori Ph.D., 医学部, 講師 (30146154)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Bi liary atresia / Reovirus type 3 |
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| Research Abstract |
The aim of the present study was 1) to perform immunohistochemistry of livers obtained during Kasai operation for infants with biliary atresia (BA) using anti-reovirus type 3 (R3), 2) to detect the RNAs of R3 from those livers with reverse transcriptase-polymerase chain reaction and 3) to elucidate pathophysiology of biliary obstruction in the neonatal mice inoculated with R3. We summarise our results as follows ; 1) 24 of 25 livers of BA reacted with anti-R3 (Abney strain : A) polyclonal antibodies, but none with anti-R3 (Dearing strain : D) monoclonal ones probably because of these weaker staining activities. 2) M1 segment of D was detected in both 3livers of BA and 2 with non-liver disease controls. 3) The liver and choledochus of neonatal mice inoculated with R3-A developed histologically similar features with human biliary atresia such as degeneration of ductular epithelia, surrounded with mononuclear infiltration, and positive R3-A associated antigens. A recent report suggests that a part of S1 segment of R3-A may play a role in determining the tropism of this virus for ductular epithelium. Therefore we believe we should try to detect this part with reverse transcription-polymerase chain reaction. Although we could not conclude that R3 causes BA in the present study, our results strongly suggest that R3-A infection may trigger the obliterative process of sclerosing cholangitis in BA.
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