| Project/Area Number |
06670758
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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 |
Pediatrics
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
AZUMA Hiroshi Asahikawa Medical College, Department of Pediatrics, Associate, 医学部, 講師 (00167909)
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| Co-Investigator(Kenkyū-buntansha) |
OKA Toshiaki Asahikawa Medical College, Department of Pediatrics, Associate, 医学部 (30111206)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | interleukin 6 / soluble interleukin 6 receptor / cerebro spinal fluid / glioblastoma / astorcytoma / herpes simplex infection / liopolysaccharide / central nervous system infection / チリオブラストーマ |
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| Research Abstract |
In the report last year, we suggested that glioblastoma cell line T98G produce interleukin 6 (IL6) when it was infected with herpes virus type 1 (HSV1). Subsequent experiment revealed that it is not HSV infection itself but some factor contaminated in the virus preparation that induce IL6 production. Lipopolysaccharide (LPS) in low concentration dose not enhance IL6 production from T98G,but the supernatant of LPS stimulated peripheral blood mononuclear cells (PBM) culture has strong IL6 inducing activity. We could demonstrate that the supernatants of low dose LPS stimulated polymorphonuclear cell (PMN) also have the same activity. Furthermore, we could suggest that in case of PMN some factor other than IL1 may play major role for IL6 inducing activity, while IL1 may be important in case of PBM.The same results were obtained using astrocytoma cell line U373. It is interesting that PMN that may appear at inflammatory site at first are involved for the regulation of IL6 production. The change of IL6 message level in U373 cells with or without HSV1 infection is under investigation.
The immunoreactive soluble IL6 receptor (sIL6R) present in cerebrospinal fluid is shown to biologically active. Thus, we speculated that sIL6R in CSF may be present in IL6-sIL6R complex. Surprisingly, when CSFs were applied to gel filtration and IL6 and sIL6R in each fraction were assayd, no peak suggesting IL6-sIL6R complex was observed. This may suggest that only a small part of sIL6R bind to IL6 and rest of sIL6R and IL6 is present in free form.
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