Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)
Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase,...
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Veröffentlicht in: | The Journal of biological chemistry 1995-03, Vol.270 (11), p.6017-6021 |
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container_title | The Journal of biological chemistry |
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creator | Terenzi, Fulvia Díaz-Guerra, María J.M. Casado, Marta Hortelano, Sonsoles Leoni, Silvia Boscá, Lisardo |
description | Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase, exhibiting a temporal pattern of nitric oxide release that was delayed with respect to the induction elicited by bacterial lipopolysaccharide. Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium.
Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells. |
doi_str_mv | 10.1074/jbc.270.11.6017 |
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Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.270.11.6017</identifier><identifier>PMID: 7534305</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Oxidoreductases - biosynthesis ; Amino Acid Sequence ; Animals ; Apoptosis - drug effects ; Cells, Cultured ; Cytokines - pharmacology ; Dose-Response Relationship, Drug ; Enzyme Induction ; Genistein ; Growth Inhibitors - pharmacology ; Hydrogen Peroxide - metabolism ; Interferon-alpha - pharmacology ; Interferon-gamma - pharmacology ; Isoflavones - pharmacology ; Lipopolysaccharides - pharmacology ; Lipoproteins - pharmacology ; Macrophages, Peritoneal - cytology ; Macrophages, Peritoneal - drug effects ; Macrophages, Peritoneal - metabolism ; Male ; Molecular Sequence Data ; Nitric Oxide - physiology ; Nitric Oxide Synthase ; Phorbol 12,13-Dibutyrate - pharmacology ; Rats ; Structure-Activity Relationship ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>The Journal of biological chemistry, 1995-03, Vol.270 (11), p.6017-6021</ispartof><rights>1995 © 1995 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-fa6cac9b1dc2912bf69d1691d4ce293909c8ed2a53763d7694be223a79628f303</citedby><cites>FETCH-LOGICAL-c508t-fa6cac9b1dc2912bf69d1691d4ce293909c8ed2a53763d7694be223a79628f303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7534305$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Terenzi, Fulvia</creatorcontrib><creatorcontrib>Díaz-Guerra, María J.M.</creatorcontrib><creatorcontrib>Casado, Marta</creatorcontrib><creatorcontrib>Hortelano, Sonsoles</creatorcontrib><creatorcontrib>Leoni, Silvia</creatorcontrib><creatorcontrib>Boscá, Lisardo</creatorcontrib><title>Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase, exhibiting a temporal pattern of nitric oxide release that was delayed with respect to the induction elicited by bacterial lipopolysaccharide. Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium.
Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells.</description><subject>Amino Acid Oxidoreductases - biosynthesis</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Cells, Cultured</subject><subject>Cytokines - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Induction</subject><subject>Genistein</subject><subject>Growth Inhibitors - pharmacology</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Interferon-alpha - pharmacology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Isoflavones - pharmacology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lipoproteins - pharmacology</subject><subject>Macrophages, Peritoneal - cytology</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Male</subject><subject>Molecular Sequence Data</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase</subject><subject>Phorbol 12,13-Dibutyrate - pharmacology</subject><subject>Rats</subject><subject>Structure-Activity Relationship</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1LHTEUhkNpsbfadVeFQKHUxVzzMV9ZWtEq3Kr0A7oLmeTMncidyZhk1PsPunDv_-svaeReChXM4oSc875vDg9C7yiZU1LlB1eNnrMqPei8JLR6gWaU1DzjBf31Es0IYTQTrKhfozchXJF0ckF30E5V8JyTYobuPysdwVu1wgs7uhHGaA0EfDaYSQM-t9FbjS_uUhN_Xw-xUwGwGgy-9K53EfBhMkUXbMCx825adv95MjsYGCGVIeJLFbtbtQ7YDvibivir0t6NnVqm_z79-f2wv4detWoV4O323kU_T45_HJ1mi4svZ0eHi0wXpI5Zq0qttGio0UxQ1rSlMLQU1OQamOCCCF2DYargVclNVYq8Aca4qkTJ6pYTvos-bnJH764nCFH2NmhYrdQAbgqSljUjtBBJeLARpkVD8NDK0dte-bWkRD7yl4m_TPwlpfKRf3K830ZPTQ_mn34LPM0_bOadXXa31oNsrNMd9E9SxEYFicKNBS-DtjBoMMmhozTOPrvBX3kqonM</recordid><startdate>19950317</startdate><enddate>19950317</enddate><creator>Terenzi, Fulvia</creator><creator>Díaz-Guerra, María J.M.</creator><creator>Casado, Marta</creator><creator>Hortelano, Sonsoles</creator><creator>Leoni, Silvia</creator><creator>Boscá, Lisardo</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>H94</scope></search><sort><creationdate>19950317</creationdate><title>Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)</title><author>Terenzi, Fulvia ; Díaz-Guerra, María J.M. ; Casado, Marta ; Hortelano, Sonsoles ; Leoni, Silvia ; Boscá, Lisardo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-fa6cac9b1dc2912bf69d1691d4ce293909c8ed2a53763d7694be223a79628f303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Amino Acid Oxidoreductases - biosynthesis</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Cells, Cultured</topic><topic>Cytokines - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Induction</topic><topic>Genistein</topic><topic>Growth Inhibitors - pharmacology</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Interferon-alpha - pharmacology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Isoflavones - pharmacology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lipoproteins - pharmacology</topic><topic>Macrophages, Peritoneal - cytology</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Male</topic><topic>Molecular Sequence Data</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase</topic><topic>Phorbol 12,13-Dibutyrate - pharmacology</topic><topic>Rats</topic><topic>Structure-Activity Relationship</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Terenzi, Fulvia</creatorcontrib><creatorcontrib>Díaz-Guerra, María J.M.</creatorcontrib><creatorcontrib>Casado, Marta</creatorcontrib><creatorcontrib>Hortelano, Sonsoles</creatorcontrib><creatorcontrib>Leoni, Silvia</creatorcontrib><creatorcontrib>Boscá, Lisardo</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Terenzi, Fulvia</au><au>Díaz-Guerra, María J.M.</au><au>Casado, Marta</au><au>Hortelano, Sonsoles</au><au>Leoni, Silvia</au><au>Boscá, Lisardo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗)</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1995-03-17</date><risdate>1995</risdate><volume>270</volume><issue>11</issue><spage>6017</spage><epage>6021</epage><pages>6017-6021</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysSerLys4 or S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase, exhibiting a temporal pattern of nitric oxide release that was delayed with respect to the induction elicited by bacterial lipopolysaccharide. Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium.
Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>7534305</pmid><doi>10.1074/jbc.270.11.6017</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amino Acid Oxidoreductases - biosynthesis Amino Acid Sequence Animals Apoptosis - drug effects Cells, Cultured Cytokines - pharmacology Dose-Response Relationship, Drug Enzyme Induction Genistein Growth Inhibitors - pharmacology Hydrogen Peroxide - metabolism Interferon-alpha - pharmacology Interferon-gamma - pharmacology Isoflavones - pharmacology Lipopolysaccharides - pharmacology Lipoproteins - pharmacology Macrophages, Peritoneal - cytology Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - metabolism Male Molecular Sequence Data Nitric Oxide - physiology Nitric Oxide Synthase Phorbol 12,13-Dibutyrate - pharmacology Rats Structure-Activity Relationship Tumor Necrosis Factor-alpha - pharmacology |
title | Bacterial Lipopeptides Induce Nitric Oxide Synthase and Promote Apoptosis through Nitric Oxide-independent Pathways in Rat Macrophages (∗) |
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