| Project/Area Number |
04671521
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | KYOTO UNIVERSITY |
|---|
Principal Investigator |
NAKAMURA Kishiko (1993) College of Medical Technology, Kyoto University, Instructor, 医療技術短期大学部, 助手 (20115900)
高橋 隆幸 (1992) 京都大学, 医学部, 助手 (50127099)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
中村 紀士子 京都大学, 医療技術短期大学部, 助手 (20115900)
|
|---|
| Project Period (FY) |
1992 – 1993
|
| Project Status |
Completed (Fiscal Year 1993)
|
| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | CSF-producing tumor / IL-1 / IL-1 receptor antagonist / G-CSF / IL-6 / CAT assay / Transcription factor / IL-1αレセプター / 転写促進因子 |
|---|
| Research Abstract |
We have reported that tumours producing colony stimulating factor (CSF) secrete interleukin-1 (IL-1) and IL-6 in addition to CSFs. In the present study, we characterized the role of IL-1 in the cytokine production. IL-1 receptor antagonist inhibited production of G-CSF and IL-6 by around 90% in CSF-producing human lung carcinoma cell lines. Similar results were obtained with hydrocortisone which supresses IL-1 gene expression. In contrast, 15non-CSF-producing human lung carcinoma cell lines did not show detectable IL-1 production, although 7 of them were induced to produce G-CSF and IL-6 by exogenous IL-1alph. Cell lines which responded to IL-1alph including CSF-producing lines expressed receptors for IL-1alpha. From these results, CSF-producing tumours could be characterized by constitutive IL-1 production, IL-1 receptor expression and IL-1-dependent hyper-production of G-CSF and IL-6. Furthermore, the transcription factor(s) suggested as one of the cause of the abnormal IL-1alph production
|
