Production of an interleukin-8-like chemokine by cytokine-stimulated rat NRK-49F fibroblasts and its suppression by anti-inflammatory steroids
Normal rat kidney fibroblasts (NRK-49F cells) stimulated with interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) produced mainly cytokine-induced neutrophil chemoattractant (CINC) which is the rat counterpart of human gro/melanoma growth stimulatory activity. In addition, the cytokine-stimul...
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| Veröffentlicht in: | Biochemical pharmacology 1993-04, Vol.45 (7), p.1425-1430 |
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| container_title | Biochemical pharmacology |
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| creator | Hideo, Nakagawa Atsutoshi, Ikesue Sinji, Hatakeyama Hideko, Kato Takuya, Gotoda Naruyasu, Komorita Kazuyoshi, Watanabe Hisato, Miyai |
| description | Normal rat kidney fibroblasts (NRK-49F cells) stimulated with interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) produced mainly cytokine-induced neutrophil chemoattractant (CINC) which is the rat counterpart of human gro/melanoma growth stimulatory activity. In addition, the cytokine-stimulated cells produced two minor neutrophil chemoattractants which are highly related to murine macrophage inflammatory protein-2 in their NH
2-terminal amino acid sequences. IL-1β was a stronger stimulator than TNF-α, and addition of both the cytokines into the NRK-49F cell culture caused an additive stimulation for rat gro/CINC production. The anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) at 10
−9–10
−6 M significantly suppressed the production of rat gro/ CINC by the IL-1β-stimulated NRK-49F cells in a dose-dependent manner. The relative potencies of the inhibitory activity of the steroids on the rat gro/CINC production were dexamethasone > prednisolone > hydrocortisone. On the other hand, the non-steroidal anti-inflammatory drugs (indomethacin and piroxicam) at 10
−7–10
−5 M showed no apparent inhibitory effect on rat gro/CINC production by NRK-49F cells stimulated with IL-1β. |
| doi_str_mv | 10.1016/0006-2952(93)90041-T |
| format | Article |
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2-terminal amino acid sequences. IL-1β was a stronger stimulator than TNF-α, and addition of both the cytokines into the NRK-49F cell culture caused an additive stimulation for rat gro/CINC production. The anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) at 10
−9–10
−6 M significantly suppressed the production of rat gro/ CINC by the IL-1β-stimulated NRK-49F cells in a dose-dependent manner. The relative potencies of the inhibitory activity of the steroids on the rat gro/CINC production were dexamethasone > prednisolone > hydrocortisone. On the other hand, the non-steroidal anti-inflammatory drugs (indomethacin and piroxicam) at 10
−7–10
−5 M showed no apparent inhibitory effect on rat gro/CINC production by NRK-49F cells stimulated with IL-1β.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/0006-2952(93)90041-T</identifier><identifier>PMID: 8471066</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Amino Acid Sequence ; Analysis of the immune response. Humoral and cellular immunity ; Animals ; Anti-Inflammatory Agents - pharmacology ; Biological and medical sciences ; Cell Line - drug effects ; Chemokine CXCL1 ; Chemokine CXCL2 ; Chemokines, CXC ; Chemotactic Factors - biosynthesis ; Fibroblasts - drug effects ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Growth Substances - biosynthesis ; Immunobiology ; Intercellular Signaling Peptides and Proteins ; Interleukin-1 - antagonists & inhibitors ; Interleukin-1 - pharmacology ; Interleukin-8 - biosynthesis ; Lymphokines, interleukins ( function, expression) ; Molecular Sequence Data ; Rats ; Recombinant Proteins - pharmacology ; Regulatory factors and their cellular receptors ; Steroids ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Biochemical pharmacology, 1993-04, Vol.45 (7), p.1425-1430</ispartof><rights>1993</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c367t-bacb57c2d7173774e31ef1f2b9aa05d78cdcb387c5dc651023c06f5c5ff9fbfc3</citedby><cites>FETCH-LOGICAL-c367t-bacb57c2d7173774e31ef1f2b9aa05d78cdcb387c5dc651023c06f5c5ff9fbfc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0006-2952(93)90041-T$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4802199$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8471066$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hideo, Nakagawa</creatorcontrib><creatorcontrib>Atsutoshi, Ikesue</creatorcontrib><creatorcontrib>Sinji, Hatakeyama</creatorcontrib><creatorcontrib>Hideko, Kato</creatorcontrib><creatorcontrib>Takuya, Gotoda</creatorcontrib><creatorcontrib>Naruyasu, Komorita</creatorcontrib><creatorcontrib>Kazuyoshi, Watanabe</creatorcontrib><creatorcontrib>Hisato, Miyai</creatorcontrib><title>Production of an interleukin-8-like chemokine by cytokine-stimulated rat NRK-49F fibroblasts and its suppression by anti-inflammatory steroids</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Normal rat kidney fibroblasts (NRK-49F cells) stimulated with interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) produced mainly cytokine-induced neutrophil chemoattractant (CINC) which is the rat counterpart of human gro/melanoma growth stimulatory activity. In addition, the cytokine-stimulated cells produced two minor neutrophil chemoattractants which are highly related to murine macrophage inflammatory protein-2 in their NH
2-terminal amino acid sequences. IL-1β was a stronger stimulator than TNF-α, and addition of both the cytokines into the NRK-49F cell culture caused an additive stimulation for rat gro/CINC production. The anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) at 10
−9–10
−6 M significantly suppressed the production of rat gro/ CINC by the IL-1β-stimulated NRK-49F cells in a dose-dependent manner. The relative potencies of the inhibitory activity of the steroids on the rat gro/CINC production were dexamethasone > prednisolone > hydrocortisone. On the other hand, the non-steroidal anti-inflammatory drugs (indomethacin and piroxicam) at 10
−7–10
−5 M showed no apparent inhibitory effect on rat gro/CINC production by NRK-49F cells stimulated with IL-1β.</description><subject>Amino Acid Sequence</subject><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Line - drug effects</subject><subject>Chemokine CXCL1</subject><subject>Chemokine CXCL2</subject><subject>Chemokines, CXC</subject><subject>Chemotactic Factors - biosynthesis</subject><subject>Fibroblasts - drug effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Growth Substances - biosynthesis</subject><subject>Immunobiology</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Interleukin-1 - antagonists & inhibitors</subject><subject>Interleukin-1 - pharmacology</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Lymphokines, interleukins ( function, expression)</subject><subject>Molecular Sequence Data</subject><subject>Rats</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Regulatory factors and their cellular receptors</subject><subject>Steroids</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc-KFDEQxoMo67j6Bgo5iOghmvSfpHMRZHFVXFRkPId0pYJxuztjkhbmJXxmMzvDHD1VqupXX4WvCHkq-GvBhXzDOZes0X3zUrevNOedYNt7ZCMG1dayHO6TzRl5SB7l_OuQDlJckIuhU4JLuSF_v6XoVighLjR6ahcaloJpwvU2LGxgU7hFCj9xjjVHOu4p7Mvdm-US5nWyBR1NttAv3z-zTl9TH8YUx8nmkquco6HGvO52CXM-bKkSdimBhcVPdp5tiWlPc90Zg8uPyQNvp4xPTvGS_Lh-v736yG6-fvh09e6GQStVYaOFsVfQOCVUq1SHrUAvfDNqa3nv1AAOxnZQ0DuQveBNC1z6HnrvtR89tJfkxVF3l-LvFXMxc8iA02QXjGs2qpdKd52sYHcEIcWcE3qzS2G2aW8EN4czmIOp5uCx0a25O4PZ1rFnJ_11nNGdh06-1_7zU99msJNPdoGQz1g38EZoXbG3RwyrF38CJpMh4ALoQkIoxsXw_3_8A6hgp2s</recordid><startdate>19930406</startdate><enddate>19930406</enddate><creator>Hideo, Nakagawa</creator><creator>Atsutoshi, Ikesue</creator><creator>Sinji, Hatakeyama</creator><creator>Hideko, Kato</creator><creator>Takuya, Gotoda</creator><creator>Naruyasu, Komorita</creator><creator>Kazuyoshi, Watanabe</creator><creator>Hisato, Miyai</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19930406</creationdate><title>Production of an interleukin-8-like chemokine by cytokine-stimulated rat NRK-49F fibroblasts and its suppression by anti-inflammatory steroids</title><author>Hideo, Nakagawa ; Atsutoshi, Ikesue ; Sinji, Hatakeyama ; Hideko, Kato ; Takuya, Gotoda ; Naruyasu, Komorita ; Kazuyoshi, Watanabe ; Hisato, Miyai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c367t-bacb57c2d7173774e31ef1f2b9aa05d78cdcb387c5dc651023c06f5c5ff9fbfc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Amino Acid Sequence</topic><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Line - drug effects</topic><topic>Chemokine CXCL1</topic><topic>Chemokine CXCL2</topic><topic>Chemokines, CXC</topic><topic>Chemotactic Factors - biosynthesis</topic><topic>Fibroblasts - drug effects</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Growth Substances - biosynthesis</topic><topic>Immunobiology</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Interleukin-1 - antagonists & inhibitors</topic><topic>Interleukin-1 - pharmacology</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Lymphokines, interleukins ( function, expression)</topic><topic>Molecular Sequence Data</topic><topic>Rats</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Regulatory factors and their cellular receptors</topic><topic>Steroids</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hideo, Nakagawa</creatorcontrib><creatorcontrib>Atsutoshi, Ikesue</creatorcontrib><creatorcontrib>Sinji, Hatakeyama</creatorcontrib><creatorcontrib>Hideko, Kato</creatorcontrib><creatorcontrib>Takuya, Gotoda</creatorcontrib><creatorcontrib>Naruyasu, Komorita</creatorcontrib><creatorcontrib>Kazuyoshi, Watanabe</creatorcontrib><creatorcontrib>Hisato, Miyai</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 pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hideo, Nakagawa</au><au>Atsutoshi, Ikesue</au><au>Sinji, Hatakeyama</au><au>Hideko, Kato</au><au>Takuya, Gotoda</au><au>Naruyasu, Komorita</au><au>Kazuyoshi, Watanabe</au><au>Hisato, Miyai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Production of an interleukin-8-like chemokine by cytokine-stimulated rat NRK-49F fibroblasts and its suppression by anti-inflammatory steroids</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>1993-04-06</date><risdate>1993</risdate><volume>45</volume><issue>7</issue><spage>1425</spage><epage>1430</epage><pages>1425-1430</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Normal rat kidney fibroblasts (NRK-49F cells) stimulated with interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) produced mainly cytokine-induced neutrophil chemoattractant (CINC) which is the rat counterpart of human gro/melanoma growth stimulatory activity. In addition, the cytokine-stimulated cells produced two minor neutrophil chemoattractants which are highly related to murine macrophage inflammatory protein-2 in their NH
2-terminal amino acid sequences. IL-1β was a stronger stimulator than TNF-α, and addition of both the cytokines into the NRK-49F cell culture caused an additive stimulation for rat gro/CINC production. The anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) at 10
−9–10
−6 M significantly suppressed the production of rat gro/ CINC by the IL-1β-stimulated NRK-49F cells in a dose-dependent manner. The relative potencies of the inhibitory activity of the steroids on the rat gro/CINC production were dexamethasone > prednisolone > hydrocortisone. On the other hand, the non-steroidal anti-inflammatory drugs (indomethacin and piroxicam) at 10
−7–10
−5 M showed no apparent inhibitory effect on rat gro/CINC production by NRK-49F cells stimulated with IL-1β.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8471066</pmid><doi>10.1016/0006-2952(93)90041-T</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Biochemical pharmacology, 1993-04, Vol.45 (7), p.1425-1430 |
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| subjects | Amino Acid Sequence Analysis of the immune response. Humoral and cellular immunity Animals Anti-Inflammatory Agents - pharmacology Biological and medical sciences Cell Line - drug effects Chemokine CXCL1 Chemokine CXCL2 Chemokines, CXC Chemotactic Factors - biosynthesis Fibroblasts - drug effects Fundamental and applied biological sciences. Psychology Fundamental immunology Growth Substances - biosynthesis Immunobiology Intercellular Signaling Peptides and Proteins Interleukin-1 - antagonists & inhibitors Interleukin-1 - pharmacology Interleukin-8 - biosynthesis Lymphokines, interleukins ( function, expression) Molecular Sequence Data Rats Recombinant Proteins - pharmacology Regulatory factors and their cellular receptors Steroids Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - pharmacology |
| title | Production of an interleukin-8-like chemokine by cytokine-stimulated rat NRK-49F fibroblasts and its suppression by anti-inflammatory steroids |
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