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Tumor Necrosis Factor (TNF)—α—Induced Interleukin-8 in Human Blood Cultures Discriminates Neutralization by the p55 and p75 TNF Soluble Receptors
The dose-dependent increase in mortality in patients with sepsis who are treated with tumor necrosis factor (TNF) p75 soluble receptor Fc conjugate (p75-Fc) remains unexplained. In this study, neutralization of TNF-α—induced interleukin (IL)—8 by p75-Fc in whole human blood exhibited a U-shaped inhi...
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| Published in: | The Journal of infectious diseases 2000-12, Vol.182 (6), p.1722-1730 |
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| container_end_page | 1730 |
| container_issue | 6 |
| container_start_page | 1722 |
| container_title | The Journal of infectious diseases |
| container_volume | 182 |
| creator | Frishman, Jordan I. Edwards, Carl K. Sonnenberg, Michael G. Kohno, Tadahiko Cohen, Arthur M. Dinarello, Charles A. |
| description | The dose-dependent increase in mortality in patients with sepsis who are treated with tumor necrosis factor (TNF) p75 soluble receptor Fc conjugate (p75-Fc) remains unexplained. In this study, neutralization of TNF-α—induced interleukin (IL)—8 by p75-Fc in whole human blood exhibited a U-shaped inhibition curve, whereas the TNF-soluble p55 receptor, linked to polyethylene glycol (p55-PEG), exhibited a dose-dependent inhibition. Native soluble p75 increased TNF-α—induced IL-8, versus a 61% reduction by native p55. Spontaneous IL-8 production was increased by p75-Fc or native p75 but not by p55-PEG or native p55. Unexpectedly, TNF-α—stimulated IL-1 receptor antagonist was suppressed by p75-Fc but not by p55-PEG. Studies of binding to TNF trimer revealed that p75-Fc has an affinity 40-fold lower than that of p55-PEG and a faster off rate. Native and p75-Fc pass TNF-α to membrane receptors more readily than does native or p55-PEG, which may partly explain the increased mortality in patients with sepsis who are treated with p75-Fc. |
| doi_str_mv | 10.1086/317605 |
| format | article |
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In this study, neutralization of TNF-α—induced interleukin (IL)—8 by p75-Fc in whole human blood exhibited a U-shaped inhibition curve, whereas the TNF-soluble p55 receptor, linked to polyethylene glycol (p55-PEG), exhibited a dose-dependent inhibition. Native soluble p75 increased TNF-α—induced IL-8, versus a 61% reduction by native p55. Spontaneous IL-8 production was increased by p75-Fc or native p75 but not by p55-PEG or native p55. Unexpectedly, TNF-α—stimulated IL-1 receptor antagonist was suppressed by p75-Fc but not by p55-PEG. Studies of binding to TNF trimer revealed that p75-Fc has an affinity 40-fold lower than that of p55-PEG and a faster off rate. Native and p75-Fc pass TNF-α to membrane receptors more readily than does native or p55-PEG, which may partly explain the increased mortality in patients with sepsis who are treated with p75-Fc.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/317605</identifier><identifier>PMID: 11069245</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>Antibacterial agents ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; Antigens, CD - immunology ; Biological and medical sciences ; Blood ; Blood Cells - drug effects ; Blood Cells - immunology ; Cells, Cultured ; Cytokines ; Dose-Response Relationship, Drug ; Human viral diseases ; Humans ; Infectious diseases ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-8 - analysis ; Interleukin-8 - immunology ; Interleukins ; Ligands ; Major Articles ; Medical sciences ; Mortality ; Neutralization Tests ; Pharmacology. Drug treatments ; Polyethylene Glycols ; Receptors ; Receptors, Tumor Necrosis Factor - immunology ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; Recombinant Fusion Proteins - immunology ; Sepsis ; Sialoglycoproteins - analysis ; Sialoglycoproteins - immunology ; Trimers ; Tumor necrosis factor receptors ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factors ; Viral diseases ; Viral diseases of the lymphoid tissue and the blood. 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Antiparasitic agents</subject><subject>Antigens, CD - immunology</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Blood Cells - drug effects</subject><subject>Blood Cells - immunology</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Dose-Response Relationship, Drug</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Interleukin 1 Receptor Antagonist Protein</subject><subject>Interleukin-8 - analysis</subject><subject>Interleukin-8 - immunology</subject><subject>Interleukins</subject><subject>Ligands</subject><subject>Major Articles</subject><subject>Medical sciences</subject><subject>Mortality</subject><subject>Neutralization Tests</subject><subject>Pharmacology. Drug treatments</subject><subject>Polyethylene Glycols</subject><subject>Receptors</subject><subject>Receptors, Tumor Necrosis Factor - immunology</subject><subject>Receptors, Tumor Necrosis Factor, Type I</subject><subject>Receptors, Tumor Necrosis Factor, Type II</subject><subject>Recombinant Fusion Proteins - immunology</subject><subject>Sepsis</subject><subject>Sialoglycoproteins - analysis</subject><subject>Sialoglycoproteins - immunology</subject><subject>Trimers</subject><subject>Tumor necrosis factor receptors</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factors</subject><subject>Viral diseases</subject><subject>Viral diseases of the lymphoid tissue and the blood. 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Antiinfectious agents. Antiparasitic agents</topic><topic>Antigens, CD - immunology</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Blood Cells - drug effects</topic><topic>Blood Cells - immunology</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Dose-Response Relationship, Drug</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Interleukin 1 Receptor Antagonist Protein</topic><topic>Interleukin-8 - analysis</topic><topic>Interleukin-8 - immunology</topic><topic>Interleukins</topic><topic>Ligands</topic><topic>Major Articles</topic><topic>Medical sciences</topic><topic>Mortality</topic><topic>Neutralization Tests</topic><topic>Pharmacology. Drug treatments</topic><topic>Polyethylene Glycols</topic><topic>Receptors</topic><topic>Receptors, Tumor Necrosis Factor - immunology</topic><topic>Receptors, Tumor Necrosis Factor, Type I</topic><topic>Receptors, Tumor Necrosis Factor, Type II</topic><topic>Recombinant Fusion Proteins - immunology</topic><topic>Sepsis</topic><topic>Sialoglycoproteins - analysis</topic><topic>Sialoglycoproteins - immunology</topic><topic>Trimers</topic><topic>Tumor necrosis factor receptors</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factors</topic><topic>Viral diseases</topic><topic>Viral diseases of the lymphoid tissue and the blood. Aids</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frishman, Jordan I.</creatorcontrib><creatorcontrib>Edwards, Carl K.</creatorcontrib><creatorcontrib>Sonnenberg, Michael G.</creatorcontrib><creatorcontrib>Kohno, Tadahiko</creatorcontrib><creatorcontrib>Cohen, Arthur M.</creatorcontrib><creatorcontrib>Dinarello, Charles A.</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frishman, Jordan I.</au><au>Edwards, Carl K.</au><au>Sonnenberg, Michael G.</au><au>Kohno, Tadahiko</au><au>Cohen, Arthur M.</au><au>Dinarello, Charles A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor Necrosis Factor (TNF)—α—Induced Interleukin-8 in Human Blood Cultures Discriminates Neutralization by the p55 and p75 TNF Soluble Receptors</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>The Journal of Infectious Diseases</addtitle><date>2000-12-01</date><risdate>2000</risdate><volume>182</volume><issue>6</issue><spage>1722</spage><epage>1730</epage><pages>1722-1730</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>The dose-dependent increase in mortality in patients with sepsis who are treated with tumor necrosis factor (TNF) p75 soluble receptor Fc conjugate (p75-Fc) remains unexplained. In this study, neutralization of TNF-α—induced interleukin (IL)—8 by p75-Fc in whole human blood exhibited a U-shaped inhibition curve, whereas the TNF-soluble p55 receptor, linked to polyethylene glycol (p55-PEG), exhibited a dose-dependent inhibition. Native soluble p75 increased TNF-α—induced IL-8, versus a 61% reduction by native p55. Spontaneous IL-8 production was increased by p75-Fc or native p75 but not by p55-PEG or native p55. Unexpectedly, TNF-α—stimulated IL-1 receptor antagonist was suppressed by p75-Fc but not by p55-PEG. Studies of binding to TNF trimer revealed that p75-Fc has an affinity 40-fold lower than that of p55-PEG and a faster off rate. Native and p75-Fc pass TNF-α to membrane receptors more readily than does native or p55-PEG, which may partly explain the increased mortality in patients with sepsis who are treated with p75-Fc.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>11069245</pmid><doi>10.1086/317605</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0022-1899 |
| ispartof | The Journal of infectious diseases, 2000-12, Vol.182 (6), p.1722-1730 |
| issn | 0022-1899 1537-6613 |
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| source | JSTOR Archival Journals and Primary Sources Collection; Oxford Journals Online |
| subjects | Antibacterial agents Antibiotics. Antiinfectious agents. Antiparasitic agents Antigens, CD - immunology Biological and medical sciences Blood Blood Cells - drug effects Blood Cells - immunology Cells, Cultured Cytokines Dose-Response Relationship, Drug Human viral diseases Humans Infectious diseases Interleukin 1 Receptor Antagonist Protein Interleukin-8 - analysis Interleukin-8 - immunology Interleukins Ligands Major Articles Medical sciences Mortality Neutralization Tests Pharmacology. Drug treatments Polyethylene Glycols Receptors Receptors, Tumor Necrosis Factor - immunology Receptors, Tumor Necrosis Factor, Type I Receptors, Tumor Necrosis Factor, Type II Recombinant Fusion Proteins - immunology Sepsis Sialoglycoproteins - analysis Sialoglycoproteins - immunology Trimers Tumor necrosis factor receptors Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factors Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids |
| title | Tumor Necrosis Factor (TNF)—α—Induced Interleukin-8 in Human Blood Cultures Discriminates Neutralization by the p55 and p75 TNF Soluble Receptors |
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