| Project/Area Number |
02670659
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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 |
Orthopaedic surgery
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| Research Institution | Kyushu Uniersity |
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Principal Investigator |
MIYAHARA Hisaaki Faculty of Medicine, Kyushu University Assistant, 医学部, 助手 (10209934)
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| Co-Investigator(Kenkyū-buntansha) |
MOHTAI Masaaki Faculty of Medicine, Kyushu University Resident, 医学部, 医員
HOTOKEBUCHI Takao Faculty of Medicine, Kyushu University Assistant, 医学部, 助手 (40190219)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | rheumatoid arthritis / ICAM-1 / HLA-DQ / adhesion molecules / collagen-induced arthritis / G-CSF / neutrophils |
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| Research Abstract |
1) Synovial tissues from inflamed joints of patients with rheumatoid arthritis and non-inflamed joints of patients with other diseases were examined for activation of vascular endothelial cells ; endothelial cells were examined for ICAM-1 expression or HLA-DQ antigen expression using immunohistologic techniques, and in situ quantification of ICAM-1 molecules was made using an immunogold method. In non-inflamed synovium, all of the endothelial cells were morphologically flat and high endothelial venutes could not be seen. Immunohistochemistry revealed that ICAM-1 molecules were expressed in approximately half number of endothelial cells. In contrast, in rheumatoid synovium, many endothelial cells altered to resemble high endothelial venutes and most of them expressed ICAM-1 on their surfaces. Immunoelectron microscopic analysis using immunogold method also revealed that ICAM-1 expression was increased in rheumatoid synovium. It was suggested that enhanced leukocytes adhesion to ondothel
… More
ial cells would occur in rheumatoid synovium in response to the increase of ICAM-1 exprcssion. On the other hand, HLA-DQ antigen expression was not detected on endothelial cells in rheumatoid or non-inflamed synovium. Further work is needed to define the expression of HLA-DQ antigen.
2) The role of neutrophils in the induction of passive arthritis with anti-type II collagen antisera was investigated. In cyclophosphamide-induced neutropenic rats, swelling and inflammation associated with the arthritic response were significantly reduced. Admninistration of 250 mug/kg of granulocyte colony-stimulating factor (G-CSF) to neutropenic rats for 7 consecutive days from the day afler cyclophosphamide injection resulted in the recovery of peripheral blood neutrophil count and the significant increase of the incidence and the severity of passive arthritis. Further study demonstrated that a prior administration of 250 mug/kg of G-CSF to naive rats for 3 consecutive days resulted in the significant enhancement of passive arthritis. It was suggested that neutrophils played an important role in the induction of passive arthritis. Less
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