About: Ketamine inhibits tumor necrosis factor secretion by RAW264.7 murine macrophages stimulated with antibiotic-exposed strains of community-associated, methicillin-resistant Staphylococcus aureus

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About: Ketamine inhibits tumor necrosis factor secretion by RAW264.7 murine macrophages stimulated with antibiotic-exposed strains of community-associated, methicillin-resistant Staphylococcus aureus Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Ketamine inhibits tumor necrosis factor secretion by RAW264.7 murine macrophages stimulated with antibiotic-exposed strains of community-associated, methicillin-resistant Staphylococcus aureus
Creator	Walker, Brett Aguirre, Carlos English, Keith Kh, Rebekah Lazar, Lauren Meals, Elizabeth Rayburn, Mark Spentzas, Thomas
topic	covid:960d26b871399621a1c32ff4b8459429893caf18#this
Source	PMC
abstract	BACKGROUND: Infections caused by community-associated strains of methicillin-resistant Staphylococcus aureus (CA-MRSA) are associated with a marked and prolonged host inflammatory response. In a sepsis simulation model, we tested whether the anesthetic ketamine inhibits the macrophage TNF response to antibiotic-exposed CA-MRSA bacteria via its antagonism of N-methyl-D-aspartate (NMDA) receptors. RAW264.7 cells were stimulated for 18 hrs with 10(5 )to 10(7 )CFU/mL inocula of either of two prototypical CA-MRSA isolates, USA300 strain LAC and USA400 strain MW2, in the presence of either vancomycin or daptomycin. One hour before bacterial stimulation, ketamine was added with or without MK-801 (dizocilpine, a chemically unrelated non-competitive NMDA receptor antagonist), APV (D-2-amino-5-phosphono-valerate, a competitive NMDA receptor antagonist), NMDA, or combinations of these agents. Supernatants were collected and assayed for TNF concentration by ELISA. RESULTS: RAW264.7 cells exposed to either LAC or MW2 in the presence of daptomycin secreted less TNF than in the presence of vancomycin. The addition of ketamine inhibited macrophage TNF secretion after stimulation with either of the CA-MRSA isolates (LAC, MW2) in the presence of either antibiotic. The NMDA inhibitors, MK-801 and APV, also suppressed macrophage TNF secretion after stimulation with either of the antibiotic-exposed CA-MRSA isolates, and the effect was not additive or synergistic with ketamine. The addition of NMDA substrate augmented TNF secretion in response to the CA-MRSA bacteria, and the addition of APV suppressed the effect of NMDA in a dose-dependent fashion. CONCLUSIONS: Ketamine inhibits TNF secretion by MRSA-stimulated RAW264.7 macrophages and the mechanism likely involves NMDA receptor antagonism. These findings may have therapeutic significance in MRSA sepsis.
has issue date	2011-01-25(xsd:dateTime)
bibo:doi	10.1186/1471-2172-12-11
bibo:pmid	21266054
has license	cc-by
sha1sum (hex)	960d26b871399621a1c32ff4b8459429893caf18
schema:url	https://doi.org/10.1186/1471-2172-12-11
resource representing a document's title	Ketamine inhibits tumor necrosis factor secretion by RAW264.7 murine macrophages stimulated with antibiotic-exposed strains of community-associated, methicillin-resistant Staphylococcus aureus
has PubMed Central identifier	PMC3037927
has PubMed identifier	21266054
schema:publication	BMC Immunol
resource representing a document's body	covid:960d26b871399621a1c32ff4b8459429893caf18#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/960d26b871399621a1c32ff4b8459429893caf18
is schema:about of	named entity 'inflammatory response' named entity 'NMDA' named entity 'ketamine' named entity 'response' named entity 'secretion' named entity 'methicillin-resistant Staphylococcus aureus' named entity 'COMPETITIVE' covid:arg/960d26b871399621a1c32ff4b8459429893caf18 named entity 'macrophage' named entity 'chemically' named entity 'CA-MRSA' named entity 'daptomycin' named entity 'ketamine' named entity 'macrophages' named entity 'ketamine' named entity 'ketamine' named entity 'bacterial infections' named entity 'MRSA' named entity 'infection' named entity 'Daptomycin' named entity 'antagonism' named entity 'bacteria' named entity 'Ketamine' named entity 'CA-MRSA' named entity 'inflammatory response' named entity 'USA300' named entity 'sepsis' named entity 'bacteria' named entity 'anesthetic' named entity 'NMDA' named entity 'antibiotic' named entity 'tumor necrosis factor' named entity 'methicillin-resistant Staphylococcus aureus' named entity 'secretion' named entity 'macrophage' named entity 'CA-MRSA' named entity 'staphylococcal infections' named entity 'Centers for Disease Control' named entity 'macrophage' named entity 'daptomycin' named entity 'macrophage' named entity 'daptomycin' named entity 'severe pneumonia' named entity 'bone marrow cells' named entity 'ketamine' named entity 'ketamine' named entity 'anti-inflammatory' named entity 'inflammatory response' named entity 'vancomycin' named entity 'staphylococci' named entity 'macrophage' named entity 'anti-inflammatory' named entity 'secretion' named entity 'NMDA' named entity 'Macrophages' named entity 'ketamine' named entity 'vancomycin' named entity 'Vancomycin' named entity 'ketamine' named entity 'lipoteichoic acid' named entity 'secretion' named entity 'MRSA' named entity 'MK-801' named entity 'CA-MRSA' named entity 'blood pressure' named entity 'macrophage' named entity 'macrophage' named entity 'antibiotics' named entity 'enzyme-linked immunosorbent assay' named entity 'secretion' named entity 'secretion' named entity 'peptidoglycan'

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