Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-8-25
pubmed:abstractText
We have investigated effects of beta-lactam antibiotics on TNF-alpha, and iNOS production from mouse peritoneal macrophages following co-culture with Escherichia coli or Staphylococcus aureus bacteria. Ceftazidime and aztreonam enhanced TNF-alpha secretion from macrophages stimulated with E. coli; however, imipenem does not alter either the kinetics or magnitude of TNF-alpha in E. coli-treated macrophages. Similar treatments with S. aureus co-cultured with macrophages markedly altered profiles of TNF-alpha response characterized by apparent early TNF-alpha peak relative to untreated S. aureus. All antibiotics increased E. coli-induced iNOS expression as assessed by both mRNA and protein. These same antibiotics significantly reduced S. aureus-induced iNOS levels of RNA. Both ceftazidime and aztreonam enhanced LPS release from E. coli in comparison to low-level LPS release from imipenem-treated bacteria, consistent with observed differences in TNF-alpha release. Incubation of all three antibiotics with S. aureus similarly increased levels of the cell wall constituent protein A detected in supernatants at early time points indicating microbial lysis. In parallel, S. aureus culture supernatants from 2-h incubation with antibiotics enhanced TNF-alpha release. These results indicate that different cellular mechanisms contribute to antibiotic-mediated regulation of TNF-alpha and iNOS secretion in mouse macrophages in response to E. coli versus S. aureus.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents, http://linkedlifedata.com/resource/pubmed/chemical/Aztreonam, http://linkedlifedata.com/resource/pubmed/chemical/Ceftazidime, http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned, http://linkedlifedata.com/resource/pubmed/chemical/Imipenem, http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Staphylococcal Protein A, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status
MEDLINE
pubmed:issn
0968-0519
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
225-36
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12935353-Animals, pubmed-meshheading:12935353-Anti-Bacterial Agents, pubmed-meshheading:12935353-Aztreonam, pubmed-meshheading:12935353-Ceftazidime, pubmed-meshheading:12935353-Cells, Cultured, pubmed-meshheading:12935353-Coculture Techniques, pubmed-meshheading:12935353-Culture Media, Conditioned, pubmed-meshheading:12935353-Escherichia coli, pubmed-meshheading:12935353-Female, pubmed-meshheading:12935353-Imipenem, pubmed-meshheading:12935353-Inflammation Mediators, pubmed-meshheading:12935353-Macrophages, Peritoneal, pubmed-meshheading:12935353-Mice, pubmed-meshheading:12935353-Mice, Inbred C3H, pubmed-meshheading:12935353-Nitric Oxide Synthase, pubmed-meshheading:12935353-Nitric Oxide Synthase Type II, pubmed-meshheading:12935353-RNA, Messenger, pubmed-meshheading:12935353-Staphylococcal Protein A, pubmed-meshheading:12935353-Staphylococcus aureus, pubmed-meshheading:12935353-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
Differential modulation of the induction of inflammatory mediators by antibiotics in mouse macrophages in response to viable Gram-positive and Gram-negative bacteria.
pubmed:affiliation
Department of Basic Medical Science, University of Missouri-Kansas City School of Medicine, Kansas City, MO 64108, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't