Differences in Release of Tumor Necrosis Factor from THP-1 Cells Stimulated by Filtrates of Antibiotic-Killed Escherichia coli
Bacterial products, such as endotoxin, activate mononuclear cells to produce tumor necrosis factor (TNF) and other monokines capable of producing host cell injury. THP-1 cell TNF release in response to bacterial products generated during antibiotic killing of Escherichia coli (ATCC 12014) was evalua...
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| Veröffentlicht in: | The Journal of infectious diseases 1991-10, Vol.164 (4), p.800-802 |
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| container_title | The Journal of infectious diseases |
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| creator | Simon, David M. Koenig, Gabriella Trenholme, Gordon M. |
| description | Bacterial products, such as endotoxin, activate mononuclear cells to produce tumor necrosis factor (TNF) and other monokines capable of producing host cell injury. THP-1 cell TNF release in response to bacterial products generated during antibiotic killing of Escherichia coli (ATCC 12014) was evaluated. THP-1 is a mature monocytic leukemia cell line that produces TNF in a dose-dependent fashion in response to purified endotoxin. E. coli were incubated in the presence of amikacin, ciprofloxacin, ceftazidime, cefotaxime, aztreonam, or imipenem at concentrations that killed >99.9% of the organisms. Aliquots of these antibiotic-bacterial cultures were added to THP-1 cells, and TNF concentrations were determined by specific immunoassay. Amikacin and imipenem produced rapid bacterial killing and were associated with low TNF levels. Ceftazidime, aztreonam, and cefotaxime killed E. coli at a slower rate and were associated with significant increases in mononuclear cell TNF responses. Ciprofloxacin produced intermediate TNF levels. Differences exist among bactericidal antibiotics in their ability to generate products capable of stimulating mononuclear cell TNF release. |
| doi_str_mv | 10.1093/infdis/164.4.800 |
| format | Article |
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THP-1 cell TNF release in response to bacterial products generated during antibiotic killing of Escherichia coli (ATCC 12014) was evaluated. THP-1 is a mature monocytic leukemia cell line that produces TNF in a dose-dependent fashion in response to purified endotoxin. E. coli were incubated in the presence of amikacin, ciprofloxacin, ceftazidime, cefotaxime, aztreonam, or imipenem at concentrations that killed >99.9% of the organisms. Aliquots of these antibiotic-bacterial cultures were added to THP-1 cells, and TNF concentrations were determined by specific immunoassay. Amikacin and imipenem produced rapid bacterial killing and were associated with low TNF levels. Ceftazidime, aztreonam, and cefotaxime killed E. coli at a slower rate and were associated with significant increases in mononuclear cell TNF responses. Ciprofloxacin produced intermediate TNF levels. Differences exist among bactericidal antibiotics in their ability to generate products capable of stimulating mononuclear cell TNF release.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/164.4.800</identifier><identifier>PMID: 1894940</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: University of Chicago Press</publisher><subject>Amikacin - pharmacology ; Anti-Bacterial Agents - pharmacology ; Antibiotics ; Aztreonam - pharmacology ; Bacteria ; Bacteriology ; Biological and medical sciences ; Cefotaxime - pharmacology ; Ceftazidime - pharmacology ; Cell lines ; Cell walls ; Ciprofloxacin - pharmacology ; Concise Communications ; Dose-Response Relationship, Drug ; Endotoxins ; Escherichia coli ; Escherichia coli - drug effects ; Escherichia coli meningitis ; Fundamental and applied biological sciences. Psychology ; Humans ; Imipenem - pharmacology ; Infections ; Leukemia, Monocytic, Acute ; Leukocytes, Mononuclear - metabolism ; Microbiology ; Polymyxins ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor necrosis factors</subject><ispartof>The Journal of infectious diseases, 1991-10, Vol.164 (4), p.800-802</ispartof><rights>Copyright 1991 The University of Chicago</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30111967$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30111967$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,777,781,800,27905,27906,57998,58231</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5328628$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1894940$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Simon, David M.</creatorcontrib><creatorcontrib>Koenig, Gabriella</creatorcontrib><creatorcontrib>Trenholme, Gordon M.</creatorcontrib><title>Differences in Release of Tumor Necrosis Factor from THP-1 Cells Stimulated by Filtrates of Antibiotic-Killed Escherichia coli</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>Bacterial products, such as endotoxin, activate mononuclear cells to produce tumor necrosis factor (TNF) and other monokines capable of producing host cell injury. THP-1 cell TNF release in response to bacterial products generated during antibiotic killing of Escherichia coli (ATCC 12014) was evaluated. THP-1 is a mature monocytic leukemia cell line that produces TNF in a dose-dependent fashion in response to purified endotoxin. E. coli were incubated in the presence of amikacin, ciprofloxacin, ceftazidime, cefotaxime, aztreonam, or imipenem at concentrations that killed >99.9% of the organisms. Aliquots of these antibiotic-bacterial cultures were added to THP-1 cells, and TNF concentrations were determined by specific immunoassay. Amikacin and imipenem produced rapid bacterial killing and were associated with low TNF levels. Ceftazidime, aztreonam, and cefotaxime killed E. coli at a slower rate and were associated with significant increases in mononuclear cell TNF responses. Ciprofloxacin produced intermediate TNF levels. Differences exist among bactericidal antibiotics in their ability to generate products capable of stimulating mononuclear cell TNF release.</description><subject>Amikacin - pharmacology</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Antibiotics</subject><subject>Aztreonam - pharmacology</subject><subject>Bacteria</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Cefotaxime - pharmacology</subject><subject>Ceftazidime - pharmacology</subject><subject>Cell lines</subject><subject>Cell walls</subject><subject>Ciprofloxacin - pharmacology</subject><subject>Concise Communications</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endotoxins</subject><subject>Escherichia coli</subject><subject>Escherichia coli - drug effects</subject><subject>Escherichia coli meningitis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Imipenem - pharmacology</subject><subject>Infections</subject><subject>Leukemia, Monocytic, Acute</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Microbiology</subject><subject>Polymyxins</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor necrosis factors</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkL1vFDEQxS0ECpdAT4PkAtHtxV_njzI6cgkiAgRHfRp7x4pP3t1g7xZp-Nsx4hRKqtHM--nNmyHkDWdrzpy8TGPsU73kWq3V2jL2jKz4RppOay6fkxVjQnTcOveSnNd6ZIwpqc0ZOWsz5RRbkV8fUoxYcAxYaRrpN8wIFekU6X4ZpkI_YyhTTZXuIMytj2Ua6P72a8fpFnOu9PuchiXDjD31j3SX8lxaU_84XI1z8mmaU-g-pZwbcV3DPZYU7hPQMOX0iryIkCu-PtUL8mN3vd_edndfbj5ur-66o7B27owILbntPUbWG8WFZ2CY57bdypXonXcYAHg0Ci04lAEUaB249xpAaXlB3v_1fSjTzwXrfBhSDS0_jDgt9WAEZ9I591-Qa8M415sGvj2Bix-wPzyUNEB5PJw-2_R3Jx1qgBwLjCHVJ2wjhdXC_rM51vbdJ1m2JdxpI38D38-Sjg</recordid><startdate>19911001</startdate><enddate>19911001</enddate><creator>Simon, David M.</creator><creator>Koenig, Gabriella</creator><creator>Trenholme, Gordon M.</creator><general>University of Chicago Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>19911001</creationdate><title>Differences in Release of Tumor Necrosis Factor from THP-1 Cells Stimulated by Filtrates of Antibiotic-Killed Escherichia coli</title><author>Simon, David M. ; Koenig, Gabriella ; Trenholme, Gordon M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j288t-72c0438dbef0d7412b0a70b18537142d9b9ecaa1f74e8a9e3ca4a66c1bb6aa463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Amikacin - pharmacology</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Antibiotics</topic><topic>Aztreonam - pharmacology</topic><topic>Bacteria</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Cefotaxime - pharmacology</topic><topic>Ceftazidime - pharmacology</topic><topic>Cell lines</topic><topic>Cell walls</topic><topic>Ciprofloxacin - pharmacology</topic><topic>Concise Communications</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endotoxins</topic><topic>Escherichia coli</topic><topic>Escherichia coli - drug effects</topic><topic>Escherichia coli meningitis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Imipenem - pharmacology</topic><topic>Infections</topic><topic>Leukemia, Monocytic, Acute</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Microbiology</topic><topic>Polymyxins</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor necrosis factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Simon, David M.</creatorcontrib><creatorcontrib>Koenig, Gabriella</creatorcontrib><creatorcontrib>Trenholme, Gordon M.</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</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>Simon, David M.</au><au>Koenig, Gabriella</au><au>Trenholme, Gordon M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differences in Release of Tumor Necrosis Factor from THP-1 Cells Stimulated by Filtrates of Antibiotic-Killed Escherichia coli</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>1991-10-01</date><risdate>1991</risdate><volume>164</volume><issue>4</issue><spage>800</spage><epage>802</epage><pages>800-802</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>Bacterial products, such as endotoxin, activate mononuclear cells to produce tumor necrosis factor (TNF) and other monokines capable of producing host cell injury. THP-1 cell TNF release in response to bacterial products generated during antibiotic killing of Escherichia coli (ATCC 12014) was evaluated. THP-1 is a mature monocytic leukemia cell line that produces TNF in a dose-dependent fashion in response to purified endotoxin. E. coli were incubated in the presence of amikacin, ciprofloxacin, ceftazidime, cefotaxime, aztreonam, or imipenem at concentrations that killed >99.9% of the organisms. Aliquots of these antibiotic-bacterial cultures were added to THP-1 cells, and TNF concentrations were determined by specific immunoassay. Amikacin and imipenem produced rapid bacterial killing and were associated with low TNF levels. Ceftazidime, aztreonam, and cefotaxime killed E. coli at a slower rate and were associated with significant increases in mononuclear cell TNF responses. Ciprofloxacin produced intermediate TNF levels. Differences exist among bactericidal antibiotics in their ability to generate products capable of stimulating mononuclear cell TNF release.</abstract><cop>Chicago, IL</cop><pub>University of Chicago Press</pub><pmid>1894940</pmid><doi>10.1093/infdis/164.4.800</doi><tpages>3</tpages></addata></record> |
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| source | MEDLINE; Jstor Complete Legacy |
| subjects | Amikacin - pharmacology Anti-Bacterial Agents - pharmacology Antibiotics Aztreonam - pharmacology Bacteria Bacteriology Biological and medical sciences Cefotaxime - pharmacology Ceftazidime - pharmacology Cell lines Cell walls Ciprofloxacin - pharmacology Concise Communications Dose-Response Relationship, Drug Endotoxins Escherichia coli Escherichia coli - drug effects Escherichia coli meningitis Fundamental and applied biological sciences. Psychology Humans Imipenem - pharmacology Infections Leukemia, Monocytic, Acute Leukocytes, Mononuclear - metabolism Microbiology Polymyxins Tumor Cells, Cultured Tumor Necrosis Factor-alpha - biosynthesis Tumor necrosis factors |
| title | Differences in Release of Tumor Necrosis Factor from THP-1 Cells Stimulated by Filtrates of Antibiotic-Killed Escherichia coli |
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