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Vol.49 (2003) >

Please use this identifier to cite or link to this item: http://ir.fmu.ac.jp/dspace/handle/123456789/134

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Title: Adhesion molecules and CXC chemokines in endotoxin-induced liver injury
Other Titles: Adhesion molecules and chemokines in liver injury
Authors: Ohira, Hiromasa
Abe, Kazumichi
Yokokawa, Junko
Takiguchi, Junko
Rai, Tsuyoshi
Shishido, Shoichiro
Sato, Yukio
Affiliation: 内科学第二講座
Source title: Fukushima Journal of Medical Science
Volume: 49
Issue: 1
Start page: 1
End page: 13
Issue Date: Jun-2003
Abstract: Interactions between leukocytes and sinusoidal endothelial cells are known to be involved in the pathogenesis of acute liver injury. Various adhesion molecules and chemokines play key roles in these cell-to-cell interactions, and the expression of these adhesion molecules and the production of chemokines are regulated by inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interferon-gamma (IFN-gamma). We have shown that the expression of intercellular adhesion molecule-1 (ICAM-1) on cultured rat sinusoidal endothelial cells stimulated with TNF-alpha increases in a dose-dependent manner. The number of neutrophils that adhered to sinusoidal endothelial cells pretreated with TNF-alpha also increased in a dose-dependent manner and significantly decreased upon incubation with an anti-ICAM-1 antibody. In endotoxin-induced rat liver injury, the number of neutrophils infiltrating the sinusoids increased after serum TNF-alpha, macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (CINC) reached their peak levels. In addition, the level of ICAM-1 expression on sinusoidal endothelial cells greatly increased from 8 h after exposure to endotoxin, and these cells were adhered to neutrophils that expressed both LFA-1 and Mac-1. Moreover, lipo-prostaglandin E1 (PGE1) reduced the extent of liver injury, and also reduced the number of neutrophils that infiltrated the liver, was reduced the production of MIP-2 and CINC, but not that of TNF-alpha, in rats injected with endotoxin.
Publisher: The Fukushima Society of Medical Science
Publisher (Alternative foam): 福島医学会
language: eng
URI: http://ir.fmu.ac.jp/dspace/handle/123456789/134
Full text URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/134/1/FksmJMedSci_49_p1.pdf
ISSN: 0016-2590
PubMed ID: 14603947
Rights: © 2003 The Fukushima Society of Medical Science
Appears in Collections:Vol.49 (2003)

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