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Vol.49 (2003) >

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タイトル: Adhesion molecules and CXC chemokines in endotoxin-induced liver injury
その他のタイトル: Adhesion molecules and chemokines in liver injury
著者: Ohira, Hiromasa
Abe, Kazumichi
Yokokawa, Junko
Takiguchi, Junko
Rai, Tsuyoshi
Shishido, Shoichiro
Sato, Yukio
学内所属: 内科学第二講座
誌名/書名: Fukushima Journal of Medical Science
巻: 49
号: 1
開始ページ: 1
終了ページ: 13
発行日: 2003年6月
抄録: 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.
出版者: The Fukushima Society of Medical Science
出版者(異表記): 福島医学会
本文の言語: eng
このページのURI: http://ir.fmu.ac.jp/dspace/handle/123456789/134
本文URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/134/1/FksmJMedSci_49_p1.pdf
ISSN: 0016-2590
DOI: 10.5387/fms.49.1
PubMed番号: 14603947
関連ページ: https://doi.org/10.5387/fms.49.1
権利情報: © 2003 The Fukushima Society of Medical Science
出現コレクション:Vol.49 (2003)

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FksmJMedSci_49_p1.pdf1.12 MBAdobe PDFダウンロード

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