Activation of alveolar macrophage TNF and MCP-1 expression in vivo by a synthetic peptide of C-reactive protein
Administration of multilamellar vesicles (MLV) encapsulating a synthetic peptide (RS‐83277) derived from human C‐reactive protein (CRP) augments anti‐tumor activity of murine alveolar macrophages and reduces established pulmonary metastases of experimental tumors. To explore mechanisms involved in t...
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Veröffentlicht in: | Journal of leukocyte biology 1996-03, Vol.59 (3), p.397-402 |
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creator | Barna, Barbara P. Thomassen, Mary Jane Zhou, Ping Pettay, James Singh‐Burgess, Sugatha Deodhar, Sharad D. |
description | Administration of multilamellar vesicles (MLV) encapsulating a synthetic peptide (RS‐83277) derived from human C‐reactive protein (CRP) augments anti‐tumor activity of murine alveolar macrophages and reduces established pulmonary metastases of experimental tumors. To explore mechanisms involved in these phenomena, we investigated cytokine and integrin (CD11b) expression of bronchoalveolar lavage (BAL)‐derived alveolar macrophages in control (blank MLV) and RS‐83277‐MLV‐treated C57B1 mice. Alveolar macrophage production of tumor necrosis factor α (TNF‐α) and monocyte chemoattractant bioactivity increased at 48 h after treatment with RS‐83277‐MLV but not control MLV. Chemoattractant activity was neutralized by antibody to monocyte chemoattractant protein‐1 (MCP‐1), but not irrelevant immunoglobulin G (IgG). Changes were reflected by augmented TNF‐α and MCP‐1 mRNA levels in pulmonary tissue and enhanced CD11b expression on mononuclear leukocytes derived from total lung tissue, but not on BAL‐derived alveolar macrophages. Results suggest that RS‐83277‐MLV treatment is associated with activation of alveolar macrophage TNF‐α and MCP‐1 production and up‐regulation of adhesion molecules on pulmonary mononuclear leukocytes but not on alveolar macrophages. |
doi_str_mv | 10.1002/jlb.59.3.397 |
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To explore mechanisms involved in these phenomena, we investigated cytokine and integrin (CD11b) expression of bronchoalveolar lavage (BAL)‐derived alveolar macrophages in control (blank MLV) and RS‐83277‐MLV‐treated C57B1 mice. Alveolar macrophage production of tumor necrosis factor α (TNF‐α) and monocyte chemoattractant bioactivity increased at 48 h after treatment with RS‐83277‐MLV but not control MLV. Chemoattractant activity was neutralized by antibody to monocyte chemoattractant protein‐1 (MCP‐1), but not irrelevant immunoglobulin G (IgG). Changes were reflected by augmented TNF‐α and MCP‐1 mRNA levels in pulmonary tissue and enhanced CD11b expression on mononuclear leukocytes derived from total lung tissue, but not on BAL‐derived alveolar macrophages. Results suggest that RS‐83277‐MLV treatment is associated with activation of alveolar macrophage TNF‐α and MCP‐1 production and up‐regulation of adhesion molecules on pulmonary mononuclear leukocytes but not on alveolar macrophages.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1002/jlb.59.3.397</identifier><identifier>PMID: 8604018</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>Amino Acid Sequence ; Animals ; Bronchoalveolar Lavage Fluid - cytology ; C-Reactive Protein - chemistry ; C-Reactive Protein - pharmacology ; Chemokine CCL2 - metabolism ; Chemokines - genetics ; Cytokines - genetics ; Gene Expression ; Immunologic Factors - pharmacology ; integrin ; Macrophage Activation ; Macrophages, Alveolar - immunology ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; monocyte chemoattractant protein 1 ; Peptide Fragments - pharmacology ; Peptides - pharmacology ; RNA, Messenger - genetics ; tumor necrosis factor ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Journal of leukocyte biology, 1996-03, Vol.59 (3), p.397-402</ispartof><rights>1996 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4557-5a40d969994e22b66ec30205e15ac0ede90d4b23aed2958455cb66f923a715a53</citedby></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/8604018$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barna, Barbara P.</creatorcontrib><creatorcontrib>Thomassen, Mary Jane</creatorcontrib><creatorcontrib>Zhou, Ping</creatorcontrib><creatorcontrib>Pettay, James</creatorcontrib><creatorcontrib>Singh‐Burgess, Sugatha</creatorcontrib><creatorcontrib>Deodhar, Sharad D.</creatorcontrib><title>Activation of alveolar macrophage TNF and MCP-1 expression in vivo by a synthetic peptide of C-reactive protein</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>Administration of multilamellar vesicles (MLV) encapsulating a synthetic peptide (RS‐83277) derived from human C‐reactive protein (CRP) augments anti‐tumor activity of murine alveolar macrophages and reduces established pulmonary metastases of experimental tumors. To explore mechanisms involved in these phenomena, we investigated cytokine and integrin (CD11b) expression of bronchoalveolar lavage (BAL)‐derived alveolar macrophages in control (blank MLV) and RS‐83277‐MLV‐treated C57B1 mice. Alveolar macrophage production of tumor necrosis factor α (TNF‐α) and monocyte chemoattractant bioactivity increased at 48 h after treatment with RS‐83277‐MLV but not control MLV. Chemoattractant activity was neutralized by antibody to monocyte chemoattractant protein‐1 (MCP‐1), but not irrelevant immunoglobulin G (IgG). Changes were reflected by augmented TNF‐α and MCP‐1 mRNA levels in pulmonary tissue and enhanced CD11b expression on mononuclear leukocytes derived from total lung tissue, but not on BAL‐derived alveolar macrophages. Results suggest that RS‐83277‐MLV treatment is associated with activation of alveolar macrophage TNF‐α and MCP‐1 production and up‐regulation of adhesion molecules on pulmonary mononuclear leukocytes but not on alveolar macrophages.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>C-Reactive Protein - chemistry</subject><subject>C-Reactive Protein - pharmacology</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokines - genetics</subject><subject>Cytokines - genetics</subject><subject>Gene Expression</subject><subject>Immunologic Factors - pharmacology</subject><subject>integrin</subject><subject>Macrophage Activation</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Sequence Data</subject><subject>monocyte chemoattractant protein 1</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptides - pharmacology</subject><subject>RNA, Messenger - genetics</subject><subject>tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9P2zAUxy00xArjtuskX7bTUp7jOImPJRpsqDAOcLac5JW6cn7MTpv1v8dVKo5wsuT3eZ-v9L6EfGUwZwDx1caWcyHnfM5ldkJmTPI84mnGP5EZZAmLRALwmZx7vwEAHqdwRs7yFBJg-Yx0i2owOz2YrqXdimq7w85qRxtdua5f6xekTw83VLc1vS8eI0bxf-_Q-wNvWrozu46We6qp37fDGgdT0R77wdR40BWRQ30IQNq7bkDTfiGnK209Xh7fC_J88-up-B0t_97-KRbLqEqEyCKhE6hlKqVMMI7LNMWKQwwCmdAVYI0S6qSMucY6liIPO1WAVjL8ZAER_IL8mLwh998W_aAa4yu0VrfYbb3KMpkJkacfgkykIDnLA_hzAsNhvHe4Ur0zjXZ7xUAdilChCCWk4ioUEfBvR--2bLB-g4-XD3M2zUdjcf-uS90tr2Fyfp921uZlPRqHyjfa2pAQq3Ec37JfAW0mn7Y</recordid><startdate>199603</startdate><enddate>199603</enddate><creator>Barna, Barbara P.</creator><creator>Thomassen, Mary Jane</creator><creator>Zhou, Ping</creator><creator>Pettay, James</creator><creator>Singh‐Burgess, Sugatha</creator><creator>Deodhar, Sharad D.</creator><general>Society for Leukocyte Biology</general><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><scope>7X8</scope></search><sort><creationdate>199603</creationdate><title>Activation of alveolar macrophage TNF and MCP-1 expression in vivo by a synthetic peptide of C-reactive protein</title><author>Barna, Barbara P. ; Thomassen, Mary Jane ; Zhou, Ping ; Pettay, James ; Singh‐Burgess, Sugatha ; Deodhar, Sharad D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4557-5a40d969994e22b66ec30205e15ac0ede90d4b23aed2958455cb66f923a715a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>C-Reactive Protein - chemistry</topic><topic>C-Reactive Protein - pharmacology</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokines - genetics</topic><topic>Cytokines - genetics</topic><topic>Gene Expression</topic><topic>Immunologic Factors - pharmacology</topic><topic>integrin</topic><topic>Macrophage Activation</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Sequence Data</topic><topic>monocyte chemoattractant protein 1</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptides - pharmacology</topic><topic>RNA, Messenger - genetics</topic><topic>tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Barna, Barbara P.</creatorcontrib><creatorcontrib>Thomassen, Mary Jane</creatorcontrib><creatorcontrib>Zhou, Ping</creatorcontrib><creatorcontrib>Pettay, James</creatorcontrib><creatorcontrib>Singh‐Burgess, Sugatha</creatorcontrib><creatorcontrib>Deodhar, Sharad D.</creatorcontrib><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><collection>MEDLINE - Academic</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Barna, Barbara P.</au><au>Thomassen, Mary Jane</au><au>Zhou, Ping</au><au>Pettay, James</au><au>Singh‐Burgess, Sugatha</au><au>Deodhar, Sharad D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of alveolar macrophage TNF and MCP-1 expression in vivo by a synthetic peptide of C-reactive protein</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>1996-03</date><risdate>1996</risdate><volume>59</volume><issue>3</issue><spage>397</spage><epage>402</epage><pages>397-402</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>Administration of multilamellar vesicles (MLV) encapsulating a synthetic peptide (RS‐83277) derived from human C‐reactive protein (CRP) augments anti‐tumor activity of murine alveolar macrophages and reduces established pulmonary metastases of experimental tumors. To explore mechanisms involved in these phenomena, we investigated cytokine and integrin (CD11b) expression of bronchoalveolar lavage (BAL)‐derived alveolar macrophages in control (blank MLV) and RS‐83277‐MLV‐treated C57B1 mice. Alveolar macrophage production of tumor necrosis factor α (TNF‐α) and monocyte chemoattractant bioactivity increased at 48 h after treatment with RS‐83277‐MLV but not control MLV. Chemoattractant activity was neutralized by antibody to monocyte chemoattractant protein‐1 (MCP‐1), but not irrelevant immunoglobulin G (IgG). Changes were reflected by augmented TNF‐α and MCP‐1 mRNA levels in pulmonary tissue and enhanced CD11b expression on mononuclear leukocytes derived from total lung tissue, but not on BAL‐derived alveolar macrophages. Results suggest that RS‐83277‐MLV treatment is associated with activation of alveolar macrophage TNF‐α and MCP‐1 production and up‐regulation of adhesion molecules on pulmonary mononuclear leukocytes but not on alveolar macrophages.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>8604018</pmid><doi>10.1002/jlb.59.3.397</doi><tpages>6</tpages></addata></record> |
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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE |
subjects | Amino Acid Sequence Animals Bronchoalveolar Lavage Fluid - cytology C-Reactive Protein - chemistry C-Reactive Protein - pharmacology Chemokine CCL2 - metabolism Chemokines - genetics Cytokines - genetics Gene Expression Immunologic Factors - pharmacology integrin Macrophage Activation Macrophages, Alveolar - immunology Male Mice Mice, Inbred C57BL Molecular Sequence Data monocyte chemoattractant protein 1 Peptide Fragments - pharmacology Peptides - pharmacology RNA, Messenger - genetics tumor necrosis factor Tumor Necrosis Factor-alpha - metabolism |
title | Activation of alveolar macrophage TNF and MCP-1 expression in vivo by a synthetic peptide of C-reactive protein |
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