Interaction of interferon-α with interleukin-1β or tumor necrosis factor-α on hepatitis B virus enhancer activity
The interaction of IFN-α with IL-1β or TNF-α on hepatitis B surface antigen (HBsAg) expression was analysed in hepatitis B virus (HBV)-DNA integrated PLC/PRF/5 and non-integrated HuH-7 human hepatoma cells. Secretion of HBsAg in PLC/PRF/5 cells was reduced by IFN-α, IL-1β or TNF-α, and synergistical...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1992-03, Vol.183 (2), p.904-909 |
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| creator | Hamasaki, Keisuke Nakata, Keisuke Nakao, Kazuhiko Mitsuoka, Satoru Tsutsumi, Takuya Kato, Yuji Shima, Masayoshi Ishii, Nobuko Tamaoki, Taiki Nagataki, Shigenobu |
| description | The interaction of IFN-α with IL-1β or TNF-α on hepatitis B surface antigen (HBsAg) expression was analysed in hepatitis B virus (HBV)-DNA integrated PLC/PRF/5 and non-integrated HuH-7 human hepatoma cells. Secretion of HBsAg in PLC/PRF/5 cells was reduced by IFN-α, IL-1β or TNF-α, and synergistically depressed when -α was used in combination with IL-1β or TNF-α. By Northern blot analysis, the levels of HBsAg mRNA were suppressed by IFN-α in combination with IL-1β or TNF-α. In the chloramphenicol acetyltransferase plasmid transfection assay, IFN-α in combination with IL-1β or TNF-α caused a much greater suppression of HBV enhancer activity than IFN-α, IL-1β or TNF-α alone in both hepatoma cells. These findings suggest that the interaction of IFN-α with IL-1β or TNF-α synergistically represses HBV enhancer activity, resulting in depressed expression of HBsAg. |
| doi_str_mv | 10.1016/0006-291X(92)90569-7 |
| format | Article |
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Secretion of HBsAg in PLC/PRF/5 cells was reduced by IFN-α, IL-1β or TNF-α, and synergistically depressed when -α was used in combination with IL-1β or TNF-α. By Northern blot analysis, the levels of HBsAg mRNA were suppressed by IFN-α in combination with IL-1β or TNF-α. In the chloramphenicol acetyltransferase plasmid transfection assay, IFN-α in combination with IL-1β or TNF-α caused a much greater suppression of HBV enhancer activity than IFN-α, IL-1β or TNF-α alone in both hepatoma cells. These findings suggest that the interaction of IFN-α with IL-1β or TNF-α synergistically represses HBV enhancer activity, resulting in depressed expression of HBsAg.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/0006-291X(92)90569-7</identifier><identifier>PMID: 1312844</identifier><identifier>CODEN: BBRCA9</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Antibiotics. 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Secretion of HBsAg in PLC/PRF/5 cells was reduced by IFN-α, IL-1β or TNF-α, and synergistically depressed when -α was used in combination with IL-1β or TNF-α. By Northern blot analysis, the levels of HBsAg mRNA were suppressed by IFN-α in combination with IL-1β or TNF-α. In the chloramphenicol acetyltransferase plasmid transfection assay, IFN-α in combination with IL-1β or TNF-α caused a much greater suppression of HBV enhancer activity than IFN-α, IL-1β or TNF-α alone in both hepatoma cells. These findings suggest that the interaction of IFN-α with IL-1β or TNF-α synergistically represses HBV enhancer activity, resulting in depressed expression of HBsAg.</description><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antiviral agents</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - microbiology</subject><subject>Chloramphenicol O-Acetyltransferase</subject><subject>Cytokines - pharmacology</subject><subject>Hepatitis B e Antigens - drug effects</subject><subject>Hepatitis B e Antigens - metabolism</subject><subject>Hepatitis B virus - drug effects</subject><subject>Hepatitis B virus - metabolism</subject><subject>Humans</subject><subject>Interferon-alpha - pharmacology</subject><subject>Interleukin-1 - pharmacology</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - microbiology</subject><subject>Medical sciences</subject><subject>Pharmacology. 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Antiinfectious agents. Antiparasitic agents</topic><topic>Antiviral agents</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - microbiology</topic><topic>Chloramphenicol O-Acetyltransferase</topic><topic>Cytokines - pharmacology</topic><topic>Hepatitis B e Antigens - drug effects</topic><topic>Hepatitis B e Antigens - metabolism</topic><topic>Hepatitis B virus - drug effects</topic><topic>Hepatitis B virus - metabolism</topic><topic>Humans</topic><topic>Interferon-alpha - pharmacology</topic><topic>Interleukin-1 - pharmacology</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - microbiology</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Recombinant Fusion Proteins - drug effects</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>Regulatory Sequences, Nucleic Acid - drug effects</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Virus Replication - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hamasaki, Keisuke</creatorcontrib><creatorcontrib>Nakata, Keisuke</creatorcontrib><creatorcontrib>Nakao, Kazuhiko</creatorcontrib><creatorcontrib>Mitsuoka, Satoru</creatorcontrib><creatorcontrib>Tsutsumi, Takuya</creatorcontrib><creatorcontrib>Kato, Yuji</creatorcontrib><creatorcontrib>Shima, Masayoshi</creatorcontrib><creatorcontrib>Ishii, Nobuko</creatorcontrib><creatorcontrib>Tamaoki, Taiki</creatorcontrib><creatorcontrib>Nagataki, Shigenobu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hamasaki, Keisuke</au><au>Nakata, Keisuke</au><au>Nakao, Kazuhiko</au><au>Mitsuoka, Satoru</au><au>Tsutsumi, Takuya</au><au>Kato, Yuji</au><au>Shima, Masayoshi</au><au>Ishii, Nobuko</au><au>Tamaoki, Taiki</au><au>Nagataki, Shigenobu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction of interferon-α with interleukin-1β or tumor necrosis factor-α on hepatitis B virus enhancer activity</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1992-03-16</date><risdate>1992</risdate><volume>183</volume><issue>2</issue><spage>904</spage><epage>909</epage><pages>904-909</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><coden>BBRCA9</coden><abstract>The interaction of IFN-α with IL-1β or TNF-α on hepatitis B surface antigen (HBsAg) expression was analysed in hepatitis B virus (HBV)-DNA integrated PLC/PRF/5 and non-integrated HuH-7 human hepatoma cells. Secretion of HBsAg in PLC/PRF/5 cells was reduced by IFN-α, IL-1β or TNF-α, and synergistically depressed when -α was used in combination with IL-1β or TNF-α. By Northern blot analysis, the levels of HBsAg mRNA were suppressed by IFN-α in combination with IL-1β or TNF-α. In the chloramphenicol acetyltransferase plasmid transfection assay, IFN-α in combination with IL-1β or TNF-α caused a much greater suppression of HBV enhancer activity than IFN-α, IL-1β or TNF-α alone in both hepatoma cells. These findings suggest that the interaction of IFN-α with IL-1β or TNF-α synergistically represses HBV enhancer activity, resulting in depressed expression of HBsAg.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>1312844</pmid><doi>10.1016/0006-291X(92)90569-7</doi><tpages>6</tpages></addata></record> |
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| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 1992-03, Vol.183 (2), p.904-909 |
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| language | eng |
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| subjects | Antibiotics. Antiinfectious agents. Antiparasitic agents Antiviral agents Biological and medical sciences Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - microbiology Chloramphenicol O-Acetyltransferase Cytokines - pharmacology Hepatitis B e Antigens - drug effects Hepatitis B e Antigens - metabolism Hepatitis B virus - drug effects Hepatitis B virus - metabolism Humans Interferon-alpha - pharmacology Interleukin-1 - pharmacology Liver Neoplasms - metabolism Liver Neoplasms - microbiology Medical sciences Pharmacology. Drug treatments Recombinant Fusion Proteins - drug effects Recombinant Fusion Proteins - metabolism Regulatory Sequences, Nucleic Acid - drug effects Transfection Tumor Cells, Cultured Tumor Necrosis Factor-alpha - pharmacology Virus Replication - drug effects |
| title | Interaction of interferon-α with interleukin-1β or tumor necrosis factor-α on hepatitis B virus enhancer activity |
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