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Role of polymorphonuclear leukocytes in galactosamine hepatitis: Mechanism of adherence to hepatic endothelial cells

✍ Scribed by Yutaka Komatsu; Yasushi Shiratori; Tateo Kawase; Naoaki Hashimoto; Katsuken Han; Shuichiro Shiina; Masayuki Matsumura; Yasuro Niwa; Naoya Kato; Minoru Tada; Yusei Ikeda; Mitsugu Tanaka; Masao Omata

Publisher: John Wiley and Sons
Year: 1994
Tongue: English
Weight: 932 KB
Volume: 20
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.1840200626

No coin nor oath required. For personal study only.

✦ Synopsis

To investigate the role of polymorphonuclear leukocytes in galactosamine-induced hepatic injury, we injected rats intraperitoneally with antiserum against rat polymorphonuclear leukocytes to deplete circulating neutrophils, then administered galactosamine plus lipopolysaccharide. Polymorphonuclear leukocytes in the hepatic sinusoids were increased after administration of galactosamine plus lipopolysaccharide, whereas pretreatment with the antiserum decreased the number of circulating leukocytes and reduced the mortality and the severity of hepatic injury. Serum collected 1 hr after galactosamine/lipopolysaccharide treatment enhanced in uitro polymorphonuclear leukocyte adherence to hepatic endothelial cells and induced leukocyte superoxide production. Intercellular adhesion molecule-1 expression on hepatic endothelial cells was also enhanced after stimulation with the serum. Polymorphonuclear leukocyte adhesion was partially inhibited by an antibody against tumor necrosis factor-a but not by superoxide dismutase. These results suggest that polymorphonuclear leukocytes play an important role in galactosamine-induced hepatic injury and that the accumulation and activation of leukocytes, as well as the enhanced expression of adhesion molecules on hepatic endothelial cells, can be induced by biologically active mediators such as tumor necrosis factor-a. In addition, prostaglandins E, and E, lessened the enhanced

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