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Cytokines in the liver
No full textCytokines comprise a group of small proteins released from cells in order to influence the function of other cells. By binding to highly specific cell-surface receptors, they trigger a vast array of intracellular signalling cascades. Cytokines have been described as interleukins, growth factors, interferons and chemokines, Unlike hormones, which act in a similar way, cytokines are produced by many different types of cell and act on many other types. Most of them are produced only after certain stimuli. The most intense field of cytokine activity is without doubt host defence. The liver resembles a central organ of cytokine activity due to the fact that it hosts hepatocytes, which are highly susceptible to the activity of cytokines in a variety of physiological and pathophysiological processes, Moreover, the non-parenchymal cells of the liver, in particular Kupffer cells (KCs), the resident tissue macrophages of the liver, are able to synthesize a variety of cytokines that may act systemically on any other organ of the body, or in a paracrine manner on hepatocytes and other nonparenchymal liver cells. A classic example of how cytokines act can be observed during the acute phase reaction discussed in this article, The role of cytokines in liver development, acute liver injury, liver regeneration, liver fibrosis and liver metastasis is also discussed. (C) 2001 Lippincott Williams & Wilkins
Follow up of three cases after adjuvant treatment of high risk gastrointestinal stromal tumors with Imatinib
No full textTwenty-six consecutive cases with progredient metastatic carcinoid tumour treated with dacarbazine: A 15-years single center experience
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Expression of osteoactivin in rat and human liver and isolated rat liver cells
No full textBackground/Aims: The transmembrane glycoprotein osteoactivin is expressed in osteoblasts, dendritic cells and tumor cells. It is suggested to influence osteoblast maturation, cell adhesion and migration. We studied osteoactivin expression within the liver. Methods: Expression of osteoactivin was analysed by RT-PCR, Northern blotting, in situ hybridisation (ISH) and immunohistochemistry (IHC) comparing normal and acutely injured rat liver [induced by carbon tetrachloride (CCl4) administration], liver cell populations, and normal or diseased human liver. Results: By ISH osteoactivin expression was detected in sinusoid-lining cells found by IHC to be positive for the common mononuclear phagocyte marker antibody anti-CD68. While total liver contained only traces, isolated Kupffer cells expressed abundant amounts of osteoactivin mRNA further increasing during culture. In acutely injured rat liver osteoactivin expression was strongly increased reaching maximum of expression 48 h after CCl4. By ISH osteoactivin expression was localised in pericentral inflammatory cells and sinusoid-lining cells again anti-CD68 positive. Dexamethasone and lipopolysaccharide decreased osteoactivin expression in cultured mononuclear phagocytes of normal as well as of acutely injured liver. In human liver osteoactivin was increased in fulminant hepatitis and paracetamol intoxication. Conclusions: Osteoactivin is expressed at high levels in normal and inflammatory liver macrophages suggesting a significant role in acute liver injury. (C) 2005 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved
Twenty-six consecutive cases with progredient metastatic carcinoid tumour treated with dacarbazine: A 15-years single center experience
No full textGadoliniumchloride treatment of rat livers induces a functional alteration but not a depletion of Kupffer cells.
No full textModulation of fibronectin gene expression in inflammatory mononuclear phagocytes of rat liver after acute liver injury
No full textBackground/Aims: In acute liver injury, fibronectin (FN) is deposited at the site of hepatocellular necrosis. We have previously shown that liver inflammatory mononuclear phagocytes (MNP), in contrast to quiescent hepatic macrophages, synthesize abundant amounts of FN. We now analyzed effects of agents known to influence macrophage functions to better understand liver damage and repair. Methods: Acute rat liver injury was induced by CCl4. Liver cellular FN (cFN) expression was analyzed by in situ-hybridization. Liver MNP were isolated and characterized immunocytochemically. Protein synthesis was studied by biosynthetic labeling, immunoprecipitation, and SDS-PAGE. RNA was analyzed by Northern Blotting. Results: cFN gene expression was localized by in situ-hybridization and immunohistochemistry within the pericentral inflammatory infiltrate. Treatment of inflammatory MNP with dexamethasone, or interferon-gamma, or lipopolysaccharide induced a dose-dependent decrease in cFN gene expression, whereas transforming growth factor-P increased cFN gene expression. Conclusions: 1. Inflammatory MNP express cFN. 2. Downregulation of cFN expression by dexamethasone in inflammatory MNP may explain delayed wound healing after corticosteroid therapy. Interferon-gamma and lipopolysaccharide could also delay the repair process in the liver. Transforming growth factor-beta may promote liver wound healing after acute liver injury by increasing local cFN synthesis in inflammatory mononuclear phagocytes of the inflammatory infiltrate. (C) 2004 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved
Successful treatment of hepatocellular carcinoma with the tyrosine kinase inhibitor imatinib in a patient with liver cirrhosis
No full textTreatment of hepatocellular carcinoma (HCC) with the tyrosine kinase inhibitor Imatinib.
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