Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin
Objective The aim of this study was to investigate whether the stimulation of monocytic cells with procalcitonin (PCT) results in the release of proinflammatory cytokines. The effects of intravenous immunoglobulin (IVIG) on the production of cytokines from the cells stimulated with PCT were also stu...
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| Veröffentlicht in: | Inflammation research 2012-06, Vol.61 (6), p.617-622 |
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| creator | Murakami, Kazuki Suzuki, Chiaki Fujii, Akihiro Imada, Teruaki |
| description | Objective
The aim of this study was to investigate whether the stimulation of monocytic cells with procalcitonin (PCT) results in the release of proinflammatory cytokines. The effects of intravenous immunoglobulin (IVIG) on the production of cytokines from the cells stimulated with PCT were also studied.
Materials and methods
Cultured monocytic cells [THP-1 cells treated with phorbol myristate acetate or peripheral blood mononuclear cells (PBMCs)] were stimulated with PCT. The protein levels of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high mobility group box-1] in the culture supernatants were determined by ELISA kits. The concentration of PCT-specific IgG antibody in IVIG was measured using a specific ELISA.
Results
PCT induced the release of cytokines from THP-1 cells in a time- and dose-dependent manner. IVIG inhibited the release of cytokines from the cells stimulated with PCT. It was confirmed that IVIG also inhibited TNF-α release in the same dose range for PBMCs stimulated with PCT. The presence of PCT-specific IgG antibody was detected in the tested IVIG, which might be one of the mechanisms.
Conclusions
PCT induced the release of proinflammatory cytokines from THP-1 cells and PBMCs. The function of PCT was prevented by the presence of IVIG. |
| doi_str_mv | 10.1007/s00011-012-0452-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1020840167</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1020840167</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-71e79a8b6e981d4f65fafa87d8483962ce7d68405e2f9db916c29c35723cd78d3</originalsourceid><addsrcrecordid>eNqNkUtrFjEUhoMotlZ_gBsJuHEzmttMMkspXgqFbix0N-TLnGlTc6lJRvlW_vWe4asiguAq4ZznfU9OXkJecvaWM6bfVcYY5x3jomOqF515RI65Eqwbmbl6jHcmZCeNZEfkWa23SBthxFNyJITsleTmmPw8S63Y75DyWqmPcU35OuTdGnyidwWw0SotEMBWoHnBWvZpCTZG23LZU7dv-atPgOJEb9ZoE405ZSx7Rx2EUGltPq7BNpjpD99uNgtng_MtJ5-ekyeLDRVePJwn5PLjhy-nn7vzi09np-_PO6dY3zrNQY_W7AYYDZ_VMvSLXazRs1FGjoNwoOfBIApiGefdyAcnRid7LaSbtZnlCXlz8MXp31aobYq-bu-zCXD1Cb-KoZ4P-j9Qzntp-rFH9PVf6G1eS8JFNkqqQXOlkOIHypVca4Fluis-2rJHaNqCnA5BThjktAU5GdS8enBedxHm34pfySEgDkDFVrqG8ufof7neA334qxg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1013467144</pqid></control><display><type>article</type><title>Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Murakami, Kazuki ; Suzuki, Chiaki ; Fujii, Akihiro ; Imada, Teruaki</creator><creatorcontrib>Murakami, Kazuki ; Suzuki, Chiaki ; Fujii, Akihiro ; Imada, Teruaki</creatorcontrib><description>Objective
The aim of this study was to investigate whether the stimulation of monocytic cells with procalcitonin (PCT) results in the release of proinflammatory cytokines. The effects of intravenous immunoglobulin (IVIG) on the production of cytokines from the cells stimulated with PCT were also studied.
Materials and methods
Cultured monocytic cells [THP-1 cells treated with phorbol myristate acetate or peripheral blood mononuclear cells (PBMCs)] were stimulated with PCT. The protein levels of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high mobility group box-1] in the culture supernatants were determined by ELISA kits. The concentration of PCT-specific IgG antibody in IVIG was measured using a specific ELISA.
Results
PCT induced the release of cytokines from THP-1 cells in a time- and dose-dependent manner. IVIG inhibited the release of cytokines from the cells stimulated with PCT. It was confirmed that IVIG also inhibited TNF-α release in the same dose range for PBMCs stimulated with PCT. The presence of PCT-specific IgG antibody was detected in the tested IVIG, which might be one of the mechanisms.
Conclusions
PCT induced the release of proinflammatory cytokines from THP-1 cells and PBMCs. The function of PCT was prevented by the presence of IVIG.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-012-0452-8</identifier><identifier>PMID: 22354318</identifier><language>eng</language><publisher>Basel: SP Birkhäuser Verlag Basel</publisher><subject>12-O-Tetradecanoylphorbol-13-acetate ; Adult ; Allergology ; Biomedical and Life Sciences ; Biomedicine ; Calcitonin - pharmacology ; Calcitonin Gene-Related Peptide ; Cell culture ; Cell Line ; Cells, Cultured ; Cytokines ; Cytokines - immunology ; Dermatology ; Enzyme-linked immunosorbent assay ; High mobility group proteins ; Humans ; Immunoglobulin G ; Immunoglobulins ; Immunoglobulins, Intravenous - pharmacology ; Immunologic Factors - pharmacology ; Immunology ; Inflammation ; Interleukin 6 ; Intravenous administration ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - immunology ; Monocytes ; Neurology ; Original Research Paper ; Peripheral blood mononuclear cells ; Pharmacology/Toxicology ; procalcitonin ; Protein Precursors - pharmacology ; Rheumatology ; Tumor necrosis factor- alpha</subject><ispartof>Inflammation research, 2012-06, Vol.61 (6), p.617-622</ispartof><rights>Springer Basel AG 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-71e79a8b6e981d4f65fafa87d8483962ce7d68405e2f9db916c29c35723cd78d3</citedby><cites>FETCH-LOGICAL-c405t-71e79a8b6e981d4f65fafa87d8483962ce7d68405e2f9db916c29c35723cd78d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00011-012-0452-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-012-0452-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22354318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murakami, Kazuki</creatorcontrib><creatorcontrib>Suzuki, Chiaki</creatorcontrib><creatorcontrib>Fujii, Akihiro</creatorcontrib><creatorcontrib>Imada, Teruaki</creatorcontrib><title>Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Objective
The aim of this study was to investigate whether the stimulation of monocytic cells with procalcitonin (PCT) results in the release of proinflammatory cytokines. The effects of intravenous immunoglobulin (IVIG) on the production of cytokines from the cells stimulated with PCT were also studied.
Materials and methods
Cultured monocytic cells [THP-1 cells treated with phorbol myristate acetate or peripheral blood mononuclear cells (PBMCs)] were stimulated with PCT. The protein levels of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high mobility group box-1] in the culture supernatants were determined by ELISA kits. The concentration of PCT-specific IgG antibody in IVIG was measured using a specific ELISA.
Results
PCT induced the release of cytokines from THP-1 cells in a time- and dose-dependent manner. IVIG inhibited the release of cytokines from the cells stimulated with PCT. It was confirmed that IVIG also inhibited TNF-α release in the same dose range for PBMCs stimulated with PCT. The presence of PCT-specific IgG antibody was detected in the tested IVIG, which might be one of the mechanisms.
Conclusions
PCT induced the release of proinflammatory cytokines from THP-1 cells and PBMCs. The function of PCT was prevented by the presence of IVIG.</description><subject>12-O-Tetradecanoylphorbol-13-acetate</subject><subject>Adult</subject><subject>Allergology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcitonin - pharmacology</subject><subject>Calcitonin Gene-Related Peptide</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Cytokines - immunology</subject><subject>Dermatology</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>High mobility group proteins</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulins</subject><subject>Immunoglobulins, Intravenous - pharmacology</subject><subject>Immunologic Factors - pharmacology</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Intravenous administration</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Monocytes</subject><subject>Neurology</subject><subject>Original Research Paper</subject><subject>Peripheral blood mononuclear cells</subject><subject>Pharmacology/Toxicology</subject><subject>procalcitonin</subject><subject>Protein Precursors - pharmacology</subject><subject>Rheumatology</subject><subject>Tumor necrosis factor- alpha</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkUtrFjEUhoMotlZ_gBsJuHEzmttMMkspXgqFbix0N-TLnGlTc6lJRvlW_vWe4asiguAq4ZznfU9OXkJecvaWM6bfVcYY5x3jomOqF515RI65Eqwbmbl6jHcmZCeNZEfkWa23SBthxFNyJITsleTmmPw8S63Y75DyWqmPcU35OuTdGnyidwWw0SotEMBWoHnBWvZpCTZG23LZU7dv-atPgOJEb9ZoE405ZSx7Rx2EUGltPq7BNpjpD99uNgtng_MtJ5-ekyeLDRVePJwn5PLjhy-nn7vzi09np-_PO6dY3zrNQY_W7AYYDZ_VMvSLXazRs1FGjoNwoOfBIApiGefdyAcnRid7LaSbtZnlCXlz8MXp31aobYq-bu-zCXD1Cb-KoZ4P-j9Qzntp-rFH9PVf6G1eS8JFNkqqQXOlkOIHypVca4Fluis-2rJHaNqCnA5BThjktAU5GdS8enBedxHm34pfySEgDkDFVrqG8ufof7neA334qxg</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Murakami, Kazuki</creator><creator>Suzuki, Chiaki</creator><creator>Fujii, Akihiro</creator><creator>Imada, Teruaki</creator><general>SP Birkhäuser Verlag Basel</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20120601</creationdate><title>Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin</title><author>Murakami, Kazuki ; Suzuki, Chiaki ; Fujii, Akihiro ; Imada, Teruaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-71e79a8b6e981d4f65fafa87d8483962ce7d68405e2f9db916c29c35723cd78d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>12-O-Tetradecanoylphorbol-13-acetate</topic><topic>Adult</topic><topic>Allergology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcitonin - pharmacology</topic><topic>Calcitonin Gene-Related Peptide</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Cytokines - immunology</topic><topic>Dermatology</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>High mobility group proteins</topic><topic>Humans</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulins</topic><topic>Immunoglobulins, Intravenous - pharmacology</topic><topic>Immunologic Factors - pharmacology</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Intravenous administration</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Monocytes</topic><topic>Neurology</topic><topic>Original Research Paper</topic><topic>Peripheral blood mononuclear cells</topic><topic>Pharmacology/Toxicology</topic><topic>procalcitonin</topic><topic>Protein Precursors - pharmacology</topic><topic>Rheumatology</topic><topic>Tumor necrosis factor- alpha</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murakami, Kazuki</creatorcontrib><creatorcontrib>Suzuki, Chiaki</creatorcontrib><creatorcontrib>Fujii, Akihiro</creatorcontrib><creatorcontrib>Imada, Teruaki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murakami, Kazuki</au><au>Suzuki, Chiaki</au><au>Fujii, Akihiro</au><au>Imada, Teruaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>61</volume><issue>6</issue><spage>617</spage><epage>622</epage><pages>617-622</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objective
The aim of this study was to investigate whether the stimulation of monocytic cells with procalcitonin (PCT) results in the release of proinflammatory cytokines. The effects of intravenous immunoglobulin (IVIG) on the production of cytokines from the cells stimulated with PCT were also studied.
Materials and methods
Cultured monocytic cells [THP-1 cells treated with phorbol myristate acetate or peripheral blood mononuclear cells (PBMCs)] were stimulated with PCT. The protein levels of proinflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high mobility group box-1] in the culture supernatants were determined by ELISA kits. The concentration of PCT-specific IgG antibody in IVIG was measured using a specific ELISA.
Results
PCT induced the release of cytokines from THP-1 cells in a time- and dose-dependent manner. IVIG inhibited the release of cytokines from the cells stimulated with PCT. It was confirmed that IVIG also inhibited TNF-α release in the same dose range for PBMCs stimulated with PCT. The presence of PCT-specific IgG antibody was detected in the tested IVIG, which might be one of the mechanisms.
Conclusions
PCT induced the release of proinflammatory cytokines from THP-1 cells and PBMCs. The function of PCT was prevented by the presence of IVIG.</abstract><cop>Basel</cop><pub>SP Birkhäuser Verlag Basel</pub><pmid>22354318</pmid><doi>10.1007/s00011-012-0452-8</doi><tpages>6</tpages></addata></record> |
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| subjects | 12-O-Tetradecanoylphorbol-13-acetate Adult Allergology Biomedical and Life Sciences Biomedicine Calcitonin - pharmacology Calcitonin Gene-Related Peptide Cell culture Cell Line Cells, Cultured Cytokines Cytokines - immunology Dermatology Enzyme-linked immunosorbent assay High mobility group proteins Humans Immunoglobulin G Immunoglobulins Immunoglobulins, Intravenous - pharmacology Immunologic Factors - pharmacology Immunology Inflammation Interleukin 6 Intravenous administration Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - immunology Monocytes Neurology Original Research Paper Peripheral blood mononuclear cells Pharmacology/Toxicology procalcitonin Protein Precursors - pharmacology Rheumatology Tumor necrosis factor- alpha |
| title | Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin |
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