Production of chemotactic factor, interleukin-8, from hepatocytes exposed to ethanol

Shiratori, Masanori; Takada, Hiroshi; Hikiba, Yohko; Nakata, Rieko; Okano, Kenichi; Komatsu, Yutaka; Niwa, Yuki; Matsumura, Masaru; Shiina, Shuichiro; Omata, Masao; Kamii, Kazuo

doi:10.1002/hep.1840180629

Cited by 43 publications

(19 citation statements)

References 34 publications

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“…After washing, sheets were resolving medium; Flow Laboratories, Inc., Irvine, Scotland) incubated with horseradish peroxidase-labeled antibody against rabbit immunoglobulin G (Amersham Japan, Tokyo, as described previously. 9 These cells were suspended in RPMI m4730f0020…”

Section: Characterization Of Stimulatory Factor In the Kupffer Cell-mentioning

confidence: 99%

“…1640 medium at a density of 2 1 10 6 cells/mL, and chemotaxis was measured according to the methods of Onozaki et al 20 and Shiratori et al 9 In brief, the chemotactic activity of hepatocyte-and Kupffer cell-conditioned medium was measured in a modified chemotaxis chamber (Sanki Co., Tokyo, Japan) with a 5-mm membrane filter (Nucleopore, Pleasanton, CA). The conditioned medium was placed in the lower compartment and neutrophils were placed in the upper compartment, and the number of neutrophils migrating through a filter to the bottom glass of the lower compartment was counted under an inverted microscope after 3 hours of culture.…”

Section: Characterization Of Stimulatory Factor In the Kupffer Cell-mentioning

confidence: 99%

“…The produc-been clarified, rat hepatocyte production of IL-8 (cytotion of CINC by hepatocytes in the presence of the LPS-kine-induced neutrophil chemoattractant in rodents stimulated Kupffer cell-conditioned medium was re- [CINC]) is increased by chronic ethanol intake in vivo 8 duced by an antibody against interleukin 1b (IL-1b), but or by exposure to ethanol in vitro. 9 Recently, the pronot by antibodies against tumor necrosis factor a (TNF-duction of IL-8 has been shown to be regulated by ina) or LPS. These results suggest that production of CINC flammatory cytokines in vitro.…”

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confidence: 99%

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Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells

et al. 1996

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To clarify the role of intercellular communication inThe liver lobule contains parenchymal cells (hepatothe liver during accumulation of neutrophils, the re-cytes) and four types of nonparenchymal cells, i.e., In severe acute alcoholic hepatitis, the plasma levels was measured by western blotting analysis and enzyme-of endotoxin and several kinds of cytokines such as linked immunosorbent assay (ELISA), and expression of interleukin 1 (IL-1), tumor necrosis factor a (TNF-a), its messenger RNA (mRNA) was assessed by the poly-and IL-8 are reported to be increased. [4][5][6][7] Neutrophil merase chain reaction. LPS-stimulated Kupffer cell-accumulation observed around sites of hepatocyte ne- kinds of cytokines and toxic substances like oxygenfree radicals and reactive nitrogen. 11,12 Previous studies have shown that endotoxin administration induces hepatic injury in alcohol-fed rats 13Abbreviations: IL, interleukin; TNF-a, tumor necrosis factor a; CINC, cytokine-induced neutrophil chemoattractant; LPS, lipopolysaccharide; ELISA, enand that endotoxemia is common in patients with alco- CINC production by hepatocytes in vitro was analyzed

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Section: Characterization Of Stimulatory Factor In the Kupffer Cell-mentioning

confidence: 99%

Section: Characterization Of Stimulatory Factor In the Kupffer Cell-mentioning

confidence: 99%

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confidence: 99%

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Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells

et al. 1996

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“…3 The human equivalent of IL-8 has not been found in the rat, but an ILRecombinant rat MIP 2 (Biosource) has a molecular weight of 8 kd (73 amino acids) and stimulates neutrophil chemotaxis, 8-like molecule, most likely related to keratinocyte cytokine/ growth related cytokine has been detected. 6,9,10,27 Another superoxide release, and degranulation. [18][19][20] The biological activity of this particular chemokine on other cells is not known.…”

Section: Effect Of Monoclonal Antibody 1f12 On Hepatic Injury Inmentioning

confidence: 99%

Chronic Alcohol Intoxication Induces Hepatic Injury Through Enhanced Macrophage Inflammatory Protein–2 Production and Intercellular Adhesion Molecule–1 Expression in the Liver

Bautista

1997

Hepatology

158

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culosis, hepatitis, and the human immunodeficiency virus/ This study tested the hypothesis that prolonged conacquired immune deficiency syndrome. Paradoxically, sumption of alcohol directly or indirectly, through endochronic alcohol intoxication may activate some aspects of nontoxin influx in the circulation, stimulates the Kupffer specific immune defense mechanisms that could initiate hecells to produce macrophage inflammatory protein-2 patic injury and liver diseases in susceptible individuals. For (MIP 2 ) and up-regulates the expression of adhesion molexample, production of proinflammatory cytokines and cheecules, i.e., CD18 on PMNs and its counter-receptor, inmokine is enhanced following alcohol consumption and in tercellular adhesion molecule-1 (ICAM-1), on hepatic individuals with alcoholic liver disease. 1-3 It has also been cells. As a result, enhanced sequestration and cell-cell widely accepted that leukocyte infiltration of the liver is a interaction among these cell types may occur in the common feature of both alcoholic hepatitis and alcoholic cirliver, which in turn could result in altered hepatic function and hepatotoxicity. This hypothesis was tested in rhosis. These are major hepatic disorders associated with alcohol-fed, specific pathogen-free, male Sprague-Daw-excessive alcohol consumption. 4 Enhanced infiltration of inley rats. After 16 weeks of feeding, endotoxin (0.2 { 0.043 flammatory polymorphonuclear neutrophils (PMNs) into the EU/mL) and MIP 2 (625 { 100 pg/mL) were detected in liver during chronic alcohol intoxication is expected to conthe sera of alcoholic rats but not in the pair-fed rats. tribute to this phenomenon. The mechanism by which alcohol Concomitantly, serum aspartate transaminase (AST) ac-enhances the migration of PMNs into the liver may be associtivity was significantly increased. Small lipid deposition ated with ethanol-mediated alteration in the expression of and inflammatory-like changes in the liver were also ob-leukocyte cell surface receptors that promote migration of served. Isolated Kupffer cells from alcohol-fed rats re-PMNs to the sites of inflammation. [4][5][6] It has been shown that leased large amount of MIP 2 (ú600 pg/10 6 Kupffer cells/ b 2 -integrin (CD18) expression on PMNs of chronic alcoholic 24 hr) in vitro compared with Kupffer cells from pair-rats is increased after 16 weeks of ethanol feeding. 6 It has fed rats (õ150 pg/10 6 Kupffer cells/24 hr). At the same also been demonstrated that there is increased hepatic setime, the expression of CD18 and ICAM-1 on polymor-questration of PMNs in chronically alcoholic rats. 7 This is phonuclear neutrophils (PMNs) and hepatic cells was accompanied by low-level endotoxemia and priming of heincreased more than twofold. Monoclonal antibody 1F12, patic phagocytes for enhanced f-met-leu-phe-mediated suan anti-CD18 antibody, attenuated hepatic injury in peroxide release. 7 In endotoxemia, it has been demonstrated vivo, and in PMN-hepatocyte coculture in vitro in the that intercellular adhesion molecule-1 (ICAM-1) e...

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“…Shiratori et al [7] reported that a major portion of the chemotactic factors released from hépato cytes exposed to ethanol was IL-8. IL-8 is generated by a KARGER E-Mail kargcr(akarger.ch F ax+ 41 61 306 12 34 hitp:// www.karger.ch variety of immune and nonimmune cells, including mac rophages and monocytes, endothelial cells, fibroblasts, hepatocytes and neutrophils [8][9][10][11][12], It is thought that hepatocyte production of IL-8 may be important in neu trophil-mediated inflammatory processes occurring via cell-to-cell interactions.…”

Section: Introductionmentioning

confidence: 99%

Enhanced lnterleukin-8 Production by Cultured Chang Liver Cells Subjected to Ethanol Exposure and Subsequent Stimulation with Tumor Necrosis Factor-α

Ohira¹,

Obara²,

Kuroda³

et al. 1997

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We investigated the production of interleukin-8 (IL-8) and chemotactic activity released from Chang liver cells subjected to long-term treatment with ethanol (Et) and subsequent stimulation with tumor necrosis factor-α (TNF-α). Chang liver cells were cultured in the presence of 5, 50 or 100 mmol/l Et for 4 weeks and then treated with recombinant TNF-α (1, 10, 100 U/ml). The culture supernatants were assayed for IL-8 using a sandwich ELISA and chemotactic activity was measured using a chemotactic chamber. Total RNA was also extracted from these cells and IL-8 mRNA was assayed by RT-PCR. In addition, TNF-receptor expression on the Et-treated cells was analyzed by flow cytometry. IL-8 levels in supernatants of cells stimulated with 100 U/ml of TNF-α for 48 h rose significantly with increasing concentrations of Et and values obtained were as follows: 4,918 ± 244.4 pg/ml at 0 mmol/l Et, 5,335 ± 266.2 pg/ml at 5 mmol/l Et, 8,726 ± 873.4 pg/ml at 50 mmol/l Et and 9,134 ± 866.0 pg/ml at 100 mmol/l Et. The chemotactic activity also increased with increasing concentrations of Et and was almost completely suppressed by anti-IL-8 antibody. Using semiquantitative analysis of radioactivity of IL-8 mRNA using a ³²P γATP-labeled primer for IL-8 mRNA, Et-treated cells were shown to have markedly higher levels of radioactivity than untreated cells. In addition, TNF-receptor expression was significantly higher in cells treated with 100 mmol/l Et. These data suggest that long-term Et treatment of Chang liver cells stimulated with TNF-α may enhance transcription of the IL-8 gene with up-regulation of the TNF receptor.

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Production of chemotactic factor, interleukin-8, from hepatocytes exposed to ethanol

Cited by 43 publications

References 34 publications

Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells

Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells

Chronic Alcohol Intoxication Induces Hepatic Injury Through Enhanced Macrophage Inflammatory Protein–2 Production and Intercellular Adhesion Molecule–1 Expression in the Liver

Enhanced lnterleukin-8 Production by Cultured Chang Liver Cells Subjected to Ethanol Exposure and Subsequent Stimulation with Tumor Necrosis Factor-α

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