Project/Area Number |
01480180
|
Research Category |
Grant-in-Aid for General Scientific Research (B)
|
Allocation Type | Single-year Grants |
Research Field |
細菌学
|
Research Institution | Jichi Medical School |
Principal Investigator |
NAKANO Masayasu Jichi Medical School, Microbiology, Prof., 医学部, 教授 (70048958)
|
Co-Investigator(Kenkyū-buntansha) |
NAKANO Yasunobu Jichi Med. School, Microbiology, Instructor, 医学部, 助手 (70207851)
SHINOMIYA Hiroto Jichi Med. School, Microbiology, Assistant Prof, 医学部, 講師 (80162618)
TAKI Tatsuo Jichi Medical School, Microbiology, Assistant Pro, 医学部, 講師 (70049097)
|
Project Period (FY) |
1989 – 1990
|
Project Status |
Completed (Fiscal Year 1990)
|
Budget Amount *help |
¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1990: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1989: ¥3,400,000 (Direct Cost: ¥3,400,000)
|
Keywords | Lipopolysaccharide (LPS) / Cytokine / Protection against infection / Salmonella / Pseudomonas aeruginosa / 内毒素 / 菌体成分 |
Research Abstract |
1. Mechanisms of macrophage activation by bacterial lipopolysaccharide (LPS). When murine peritoneal macrophages are stimulated by LPS, the macrophages produce various kinds of cytokines, and augment their bactericidal capacity. We investigated biochemical events in the macrophages after the stimulation of LPS. Calmodulin system was relevant to the macrophage activation by LPS to produce IL-1, while protein-kinase C and cyclic AMP as well as cyclic GMP seemed to be irrelevant to it. Shortly after LPS-stimulation, some proteins in the cell membrane and cytosol of the macrophages were phosphorylated. We purified the most dominant phosphorylated protein (pp65) in the cytosol, and found that the pp 65 was a substrate of serine kinase with a structure similar to human plastin. 2. Protective role of cytokines in the bacterial infection. When some of recombinant cytokines (either IFN-gamma, TNF-alpha and beta, IL-1, IL-6, or G-CSF) was injected into mice, bactericidal capacity and protectivity in the mice against Salmonella typhimurium (or S. enteritidis) and Pseudomonas aeruginosa were augmented. Combination of some of the cytokines or cytokine plus LPS was more effective. The augmentaion was partly due to the recruitment of phagocytic cells and the increment of the phagocytic and killing abilities of individual cells.
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