Effects of cAMP-Phosphodiesterase Isozyme Inhibitor on Cytokine Production by Lipopolysaccharide-Stimulated Human Peripheral Blood Mononuclear Cells
1. The effects of cAMP-phosphodiesterase (PDE) isozyme inhibitors on the production of tumor necrosis factor α (TNF-α), and interleukins 1β and 8 (IL-1β and IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC) were evaluated. In addition, we investigated the e...
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| Veröffentlicht in: | General pharmacology 1997-10, Vol.29 (4), p.633-638 |
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| creator | Yoshimura, Tomoaki Kurita, Chikako Nagao, Tomomi Usami, Eiseki Nakao, Toshiya Watanabe, Shino Kobayashi, Joji Yamazaki, Futoshi Tanaka, Hiroyuki Nagai, Hiroichi |
| description | 1.
The effects of cAMP-phosphodiesterase (PDE) isozyme inhibitors on the production of tumor necrosis factor α (TNF-α), and interleukins 1β and 8 (IL-1β and IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC) were evaluated. In addition, we investigated the effects of dibutyryl cAMP (dbcAMP) and β-adrenergic receptor agonist on the production of these cytokines.
2.
Type IV PDE inhibitors were more effective at inhibiting the production of TNF-α and IL-1β by LPS-stimulated PBMC than a nonselective, type III or type III/IV inhibitor. In contrast, these agents had no effect on IL-8 production.
3.
Increasing concentrations of dbcAMP progressively reduced the production of TNF-α and IL-1β but not IL-8.
4.
The addition of β-agonist increased the inhibitory effect of PDE inhibitors tested on the production of TNF-α and IL-1β.
5.
Type IV PDE inhibitors could be potent pharmacological agents for the treatment of diseases in which TNF-α and IL-1β are important etiological factors. |
| doi_str_mv | 10.1016/S0306-3623(96)00580-0 |
| format | Article |
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The effects of cAMP-phosphodiesterase (PDE) isozyme inhibitors on the production of tumor necrosis factor α (TNF-α), and interleukins 1β and 8 (IL-1β and IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC) were evaluated. In addition, we investigated the effects of dibutyryl cAMP (dbcAMP) and β-adrenergic receptor agonist on the production of these cytokines.
2.
Type IV PDE inhibitors were more effective at inhibiting the production of TNF-α and IL-1β by LPS-stimulated PBMC than a nonselective, type III or type III/IV inhibitor. In contrast, these agents had no effect on IL-8 production.
3.
Increasing concentrations of dbcAMP progressively reduced the production of TNF-α and IL-1β but not IL-8.
4.
The addition of β-agonist increased the inhibitory effect of PDE inhibitors tested on the production of TNF-α and IL-1β.
5.
Type IV PDE inhibitors could be potent pharmacological agents for the treatment of diseases in which TNF-α and IL-1β are important etiological factors.</description><identifier>ISSN: 0306-3623</identifier><identifier>EISSN: 1879-0011</identifier><identifier>DOI: 10.1016/S0306-3623(96)00580-0</identifier><identifier>PMID: 9352314</identifier><identifier>CODEN: GEPHDP</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>3',5'-Cyclic-AMP Phosphodiesterases - antagonists & inhibitors ; 4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone - pharmacology ; Aminophylline - pharmacology ; Biological and medical sciences ; Bones, joints and connective tissue. Antiinflammatory agents ; Bucladesine - pharmacology ; cAMP ; Cytokines - blood ; Humans ; In Vitro Techniques ; Interleukin-1 - metabolism ; interleukin-1β ; interleukin-8 ; Interleukin-8 - metabolism ; Isoenzymes - antagonists & inhibitors ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - metabolism ; Lipopolysaccharides - pharmacology ; Medical sciences ; Milrinone ; mononuclear cells ; Naphthyridines - pharmacology ; Pharmacology. Drug treatments ; Phosphodiesterase Inhibitors - pharmacology ; Phosphodiesterase isozyme inhibitor ; Purinones - pharmacology ; Pyridones - pharmacology ; Pyrrolidinones - pharmacology ; Rolipram ; Terbutaline - pharmacology ; Tumor Necrosis Factor-alpha - metabolism ; tumor necrosis factor-α</subject><ispartof>General pharmacology, 1997-10, Vol.29 (4), p.633-638</ispartof><rights>1997 Elsevier Science Inc.</rights><rights>1997 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-fff195d0c3bec277cd64afd16e24335bada10f48d8831624d61a9541464f5ad03</citedby><cites>FETCH-LOGICAL-c507t-fff195d0c3bec277cd64afd16e24335bada10f48d8831624d61a9541464f5ad03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2838843$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9352314$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshimura, Tomoaki</creatorcontrib><creatorcontrib>Kurita, Chikako</creatorcontrib><creatorcontrib>Nagao, Tomomi</creatorcontrib><creatorcontrib>Usami, Eiseki</creatorcontrib><creatorcontrib>Nakao, Toshiya</creatorcontrib><creatorcontrib>Watanabe, Shino</creatorcontrib><creatorcontrib>Kobayashi, Joji</creatorcontrib><creatorcontrib>Yamazaki, Futoshi</creatorcontrib><creatorcontrib>Tanaka, Hiroyuki</creatorcontrib><creatorcontrib>Nagai, Hiroichi</creatorcontrib><title>Effects of cAMP-Phosphodiesterase Isozyme Inhibitor on Cytokine Production by Lipopolysaccharide-Stimulated Human Peripheral Blood Mononuclear Cells</title><title>General pharmacology</title><addtitle>Gen Pharmacol</addtitle><description>1.
The effects of cAMP-phosphodiesterase (PDE) isozyme inhibitors on the production of tumor necrosis factor α (TNF-α), and interleukins 1β and 8 (IL-1β and IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC) were evaluated. In addition, we investigated the effects of dibutyryl cAMP (dbcAMP) and β-adrenergic receptor agonist on the production of these cytokines.
2.
Type IV PDE inhibitors were more effective at inhibiting the production of TNF-α and IL-1β by LPS-stimulated PBMC than a nonselective, type III or type III/IV inhibitor. In contrast, these agents had no effect on IL-8 production.
3.
Increasing concentrations of dbcAMP progressively reduced the production of TNF-α and IL-1β but not IL-8.
4.
The addition of β-agonist increased the inhibitory effect of PDE inhibitors tested on the production of TNF-α and IL-1β.
5.
Type IV PDE inhibitors could be potent pharmacological agents for the treatment of diseases in which TNF-α and IL-1β are important etiological factors.</description><subject>3',5'-Cyclic-AMP Phosphodiesterases - antagonists & inhibitors</subject><subject>4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone - pharmacology</subject><subject>Aminophylline - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Bucladesine - pharmacology</subject><subject>cAMP</subject><subject>Cytokines - blood</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Interleukin-1 - metabolism</subject><subject>interleukin-1β</subject><subject>interleukin-8</subject><subject>Interleukin-8 - metabolism</subject><subject>Isoenzymes - antagonists & inhibitors</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Medical sciences</subject><subject>Milrinone</subject><subject>mononuclear cells</subject><subject>Naphthyridines - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphodiesterase Inhibitors - pharmacology</subject><subject>Phosphodiesterase isozyme inhibitor</subject><subject>Purinones - pharmacology</subject><subject>Pyridones - pharmacology</subject><subject>Pyrrolidinones - pharmacology</subject><subject>Rolipram</subject><subject>Terbutaline - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>tumor necrosis factor-α</subject><issn>0306-3623</issn><issn>1879-0011</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi0EKtuFR6jkA0L0EBjHsZOcUFkVWmkrViqcLcceaw1JHOwEKTwHD0y2u9orp5FmfvPv-wi5YvCeAZMfHoGDzLjM-btaXgOICjJ4RlasKusMgLHnZHVGXpLLlH4AQC7y_IJc1FzknBUr8vfWOTRjosFRc_Owy3b7kIZ9sB7TiFEnpPcp_Jm7JfZ73_gxRBp6upnH8NP3SHcx2MmMfsk1M936IQyhnZM2Zq-jt5g9jr6bWj2ipXdTp3u6w-iH_TK7pZ_aECx9CH3oJ9OijnSDbZtekRdOtwlfn-KafP98-21zl22_frnf3GwzI6AcM-ccq4UFwxs0eVkaKwvtLJOYF5yLRlvNwBWVrSrOZF5YyXQtClbIwgltga_J2-PcIYZf0_Kw6nwyywW6xzAlVda8FBIOoDiCJoaUIjo1RN_pOCsG6uCGenJDHaRWtVRPbqhD39VpwdR0aM9dJ_mX-ptTXSejWxd1b3w6Y3nFq2p5ZU0-HjFcxPjtMapkPPYGrY-LecoG_59D_gFJPKle</recordid><startdate>19971001</startdate><enddate>19971001</enddate><creator>Yoshimura, Tomoaki</creator><creator>Kurita, Chikako</creator><creator>Nagao, Tomomi</creator><creator>Usami, Eiseki</creator><creator>Nakao, Toshiya</creator><creator>Watanabe, Shino</creator><creator>Kobayashi, Joji</creator><creator>Yamazaki, Futoshi</creator><creator>Tanaka, Hiroyuki</creator><creator>Nagai, Hiroichi</creator><general>Elsevier Inc</general><general>Elsevier</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>19971001</creationdate><title>Effects of cAMP-Phosphodiesterase Isozyme Inhibitor on Cytokine Production by Lipopolysaccharide-Stimulated Human Peripheral Blood Mononuclear Cells</title><author>Yoshimura, Tomoaki ; Kurita, Chikako ; Nagao, Tomomi ; Usami, Eiseki ; Nakao, Toshiya ; Watanabe, Shino ; Kobayashi, Joji ; Yamazaki, Futoshi ; Tanaka, Hiroyuki ; Nagai, Hiroichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-fff195d0c3bec277cd64afd16e24335bada10f48d8831624d61a9541464f5ad03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>3',5'-Cyclic-AMP Phosphodiesterases - antagonists & inhibitors</topic><topic>4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone - pharmacology</topic><topic>Aminophylline - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Bucladesine - pharmacology</topic><topic>cAMP</topic><topic>Cytokines - blood</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Interleukin-1 - metabolism</topic><topic>interleukin-1β</topic><topic>interleukin-8</topic><topic>Interleukin-8 - metabolism</topic><topic>Isoenzymes - antagonists & inhibitors</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Medical sciences</topic><topic>Milrinone</topic><topic>mononuclear cells</topic><topic>Naphthyridines - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphodiesterase Inhibitors - pharmacology</topic><topic>Phosphodiesterase isozyme inhibitor</topic><topic>Purinones - pharmacology</topic><topic>Pyridones - pharmacology</topic><topic>Pyrrolidinones - pharmacology</topic><topic>Rolipram</topic><topic>Terbutaline - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>tumor necrosis factor-α</topic><toplevel>online_resources</toplevel><creatorcontrib>Yoshimura, Tomoaki</creatorcontrib><creatorcontrib>Kurita, Chikako</creatorcontrib><creatorcontrib>Nagao, Tomomi</creatorcontrib><creatorcontrib>Usami, Eiseki</creatorcontrib><creatorcontrib>Nakao, Toshiya</creatorcontrib><creatorcontrib>Watanabe, Shino</creatorcontrib><creatorcontrib>Kobayashi, Joji</creatorcontrib><creatorcontrib>Yamazaki, Futoshi</creatorcontrib><creatorcontrib>Tanaka, Hiroyuki</creatorcontrib><creatorcontrib>Nagai, Hiroichi</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>General pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshimura, Tomoaki</au><au>Kurita, Chikako</au><au>Nagao, Tomomi</au><au>Usami, Eiseki</au><au>Nakao, Toshiya</au><au>Watanabe, Shino</au><au>Kobayashi, Joji</au><au>Yamazaki, Futoshi</au><au>Tanaka, Hiroyuki</au><au>Nagai, Hiroichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of cAMP-Phosphodiesterase Isozyme Inhibitor on Cytokine Production by Lipopolysaccharide-Stimulated Human Peripheral Blood Mononuclear Cells</atitle><jtitle>General pharmacology</jtitle><addtitle>Gen Pharmacol</addtitle><date>1997-10-01</date><risdate>1997</risdate><volume>29</volume><issue>4</issue><spage>633</spage><epage>638</epage><pages>633-638</pages><issn>0306-3623</issn><eissn>1879-0011</eissn><coden>GEPHDP</coden><abstract>1.
The effects of cAMP-phosphodiesterase (PDE) isozyme inhibitors on the production of tumor necrosis factor α (TNF-α), and interleukins 1β and 8 (IL-1β and IL-8) by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC) were evaluated. In addition, we investigated the effects of dibutyryl cAMP (dbcAMP) and β-adrenergic receptor agonist on the production of these cytokines.
2.
Type IV PDE inhibitors were more effective at inhibiting the production of TNF-α and IL-1β by LPS-stimulated PBMC than a nonselective, type III or type III/IV inhibitor. In contrast, these agents had no effect on IL-8 production.
3.
Increasing concentrations of dbcAMP progressively reduced the production of TNF-α and IL-1β but not IL-8.
4.
The addition of β-agonist increased the inhibitory effect of PDE inhibitors tested on the production of TNF-α and IL-1β.
5.
Type IV PDE inhibitors could be potent pharmacological agents for the treatment of diseases in which TNF-α and IL-1β are important etiological factors.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>9352314</pmid><doi>10.1016/S0306-3623(96)00580-0</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | General pharmacology, 1997-10, Vol.29 (4), p.633-638 |
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| subjects | 3',5'-Cyclic-AMP Phosphodiesterases - antagonists & inhibitors 4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone - pharmacology Aminophylline - pharmacology Biological and medical sciences Bones, joints and connective tissue. Antiinflammatory agents Bucladesine - pharmacology cAMP Cytokines - blood Humans In Vitro Techniques Interleukin-1 - metabolism interleukin-1β interleukin-8 Interleukin-8 - metabolism Isoenzymes - antagonists & inhibitors Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - metabolism Lipopolysaccharides - pharmacology Medical sciences Milrinone mononuclear cells Naphthyridines - pharmacology Pharmacology. Drug treatments Phosphodiesterase Inhibitors - pharmacology Phosphodiesterase isozyme inhibitor Purinones - pharmacology Pyridones - pharmacology Pyrrolidinones - pharmacology Rolipram Terbutaline - pharmacology Tumor Necrosis Factor-alpha - metabolism tumor necrosis factor-α |
| title | Effects of cAMP-Phosphodiesterase Isozyme Inhibitor on Cytokine Production by Lipopolysaccharide-Stimulated Human Peripheral Blood Mononuclear Cells |
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