2005 Fiscal Year Final Research Report Summary
The role of Il-18 In Inducing or preventing apoptosis in neutrophils during acute endotoxemia
| Project/Area Number |
16591818
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
KOTANI Joji Hyogo College of Medicine, Faculty of Medicine, Research Associate, 医学部, 助手 (80360270)
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| Co-Investigator(Kenkyū-buntansha) |
OHYA Munehiko Hyogo College of Medicine, Faculty of Medicine, Research Associate, 医学部, 助手 (40309480)
OKAMURA Haruki Hyogo College of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (60111043)
MARUKAWA Seishiro Hyogo College of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (00030883)
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| Project Period (FY) |
2004 – 2005
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| Keywords | IL-18 / neutrophil / bone marrow cells / endotoxin / popy unsaturated fatty acids / mouse / rat / tumor necrosis factor |
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| Research Abstract |
1.The role of TNR receptors in bone marrow cell apoptosis during endotoxin-induced systemic inflammatory state. Apoptosis of myeloid cells in the bone marrow during endotoxemia is minimized as these cells undergo differentiation, which in turn, may be due to the attenuation of the pro-apoptotic effect of TNFR-p55 shown herein to occur with myeloid differentiation. In contrast, TNFR-p75 appears to play a minimal role in apoptosis induction in Grl(-) myeloid cells during endotoxemia. One explanation for a decrease in bone marrow cell numbers during endotoxemia may be via induction of apoptosis in immature myeloid cells.
2.The role of IL-18 in bone marrow cell apoptosis during endotoxin-induced systemic inflammatory state. It has been demonstrated that IL-18 plays a anti-apoptotic role in mature and immature myeloid cells in the bone marrow during endotoxin-induced systemic inflammatory state.
3.The role of IL-18 in both nitric oxide production and pancreatic damage during acute pancreatiti
… More
s. IL-18 appears to protect the pancreas during early caerulein-induced AP in mice, probably through induction of NO release from an iNOS source. IL-18 may be a target for new AP therapeutics.
4.Establishment of the technique of total parenteral nutrition (TPN) in rats. We have developed the techniques to insert and fix the silicon tube into the jugular vein, transfuse TPN solution for three days safely without restriction in Wister rats.
5.Apoptosis induction in the bone marrow cells during endotoxin-induced systemic inflammatory state in rats. We have confirmed that apoptosis is induced in both immature and mature bone marrow cells after intra-peritoneal injection of endotoxin like apoptosis induction in the bone marrow cells in mouse acute endotoxemia model.
6.The influence of pretreatment with TPN with n-6 and n-3 poly unsaturated fatty acids (PUFAs) on apoptosis in bone marrow cells and peripheral neutrophils during endotoxin-induced systemic inflammatory state. The HPLC analysis revealed that three days TPN could change the cell wall components of spleen cells and red blood cells. Furthermore, we have found that pretreatment with TPN with n-3 PUFAs appears to increase apoptotic cell rate in the immature and mature bone marrow cells and peripheral neutrophils compared to TPN with n-6 PUFAs although the mechanisms have not been elucidated.
7.The role of IL-18 in human neutrophils apotosis. IL-18, like LPS, inhibits PMN apoptosis by activating PI3-kinase and ERK pathways. However, PI3-kinase plays more important role(s) in IL-18-induced inhibition of apoptosis than in LPS-induced apoptosis inhibition.
8.The influence of short chain fatty acids (SCFAs). Butyrate activates caspase cascade and induces apoptosis via signal transduction(s) other than GPR and MAPKs. It is most likely that butyrate modulate apoptosis via HDAC inhibition. Less
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Research Products
(12 results)
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[Journal Article] The mechanisms of organ dysfunction during severe infection.2005
Author(s)
Joji Kotani, Jun-ichi Hirata, Masahiro Goshima, MD, PhD, Mariko Yamada, Munenori Matsudaira, Munehiko Ohya, Manabu Kirita, Kazumasa Yoshinaga, Seishiro Marukawa.
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Journal Title
日本腹部救急医学会雑誌 25(5)
Pages: 718-720
Description
「研究成果報告書概要(欧文)」より
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