2001 Fiscal Year Final Research Report Summary
Signal transduction in neutrophils under surgical stress
| Project/Area Number |
12557098
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
General surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SAITO Hideaki The Univ. of Tokyo, Faculty of Medicine, Professor, 医学部・附属病院, 教授 (30134555)
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| Co-Investigator(Kenkyū-buntansha) |
OGURA Makoto The Univ. of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (50185568)
UETERA Yuushi The Univ. of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (80191914)
CHINZEI Mieko The Univ. of Tokyo, Faculty of Medicine, Lecturer, 医学部・附属病院, 講師 (30165097)
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| Project Period (FY) |
2000 – 2001
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| Keywords | neutrophil / macrophage / malnutrition / signal transduction / thyrosine kinase / host immunity |
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| Research Abstract |
Malnutrition impairs host immunity resulting in high mortality and morbidity due to infections. Phosphorylation of protein tyrosine kinase (PTK) is a key step in the signaling of many cellular functions. Malnutrition may affect this signaling in response to surgical insults. The aim of this study was to examine effects of PTK inhibition on host immunity.
Diet restriction reduced survival of mice after cecal ligation and puncture compared with ad libitum group. Tyrosine kinase inhibition decreased survival of ad libitum mice but did not change that of diet restricted mice. Tyrosine phosphorylation in peritoneal exudative cells from mice with malnutrition was inhibited after stimulation, which may be an important mechanism for impaired host immunity accompanying to malnutrition.
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