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The close relationship between interleukin‐1 and fibroblast proliferating factor from peripheral mononuclear cells of patients with chronic hepatitis and liver cirrhosis

 

作者: YOSHIRO NIITSU,   YUTAKA KOHGO,   MANABU BUNYA,   KYUHEI KOHDA,   NOBUYUKI ITOH,   MINORU OHWADA,   KOHETSU MORITA,   KUNIHIKO MATSUURA,   NAOKI WATANABE,   ICHIRO URUSHIZAKI,  

 

期刊: Journal of Gastroenterology and Hepatology  (WILEY Available online 1988)
卷期: Volume 3, issue 1  

页码: 37-45

 

ISSN:0815-9319

 

年代: 1988

 

DOI:10.1111/j.1440-1746.1988.tb00215.x

 

出版商: Blackwell Publishing Ltd

 

关键词: chronic hepatitis;cirrhosis;fibroblast proliferating factor;hepatic fibrosis;interleukin‐1;peripheral mononuclear cells.

 

数据来源: WILEY

 

摘要:

AbstractThe role of peripheral mononuclear cells (PMNC) was investigated in patients with hepatic fibrosis of chronic hepatitis or liver cirrhosis. PMNC from these patients released more fibroblast proliferating factor (FPF) in the conditioned medium than those PMNC from normal subjects in response to PHA stimulation. Production of FPF by PMNC from CAH patients was also observed in response to liver specific protein (LSP) which might act as a naturally occurring antigenin vivo.Analysis of FPF on gel permeation chromatography revealed two active components with molecular weight of 60000 (FPF‐1) and 18000 (FPF‐II). Both FPF‐I and FPF‐II exerted thymocyte proliferating activity, but not cytotoxic T cell line (CTLL) proliferating activity, indicating that they are closely related to interleukin‐1 (IL‐1).Isoelectrofocusing of FPF‐I and FPF‐II disclosed that each factor consisted of two peaks at similar pI: 5.3 and 7.0. Taking account of the fact the IL‐1 consisted of two molecular forms of pI—5.4 (IL‐1α) and 7.0 (IL‐1β)—FPF‐II is considered to be IL‐1, which is a mixture of IL‐1α and IL‐1β, and FPF‐I is probably the aggregated form of FPF‐II.This assumption was further supported by the evidence that macrophages, which are the major source of IL‐1 in patients with chronic hepatitis or liver cirrhosis, also released significantly higher amounts of FPF than those from normal subjects in response to stimulation by lipopolysaccharide. It was therefore concluded that in chronic hepatitis and liver cirrhosis, production of an IL‐1, or a factor similar to IL‐1, by

 

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