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dc.contributor.authorBonaterra, Gabriel A.
dc.contributor.authorDriscoll, David F.
dc.contributor.authorSchwarzbach, Hans
dc.contributor.authorKinscherf, Ralf
dc.date2022-08-11T08:09:47.000
dc.date.accessioned2022-08-23T16:43:32Z
dc.date.available2022-08-23T16:43:32Z
dc.date.issued2017-03-15
dc.date.submitted2017-09-12
dc.identifier.citationMar Drugs. 2017 Mar 15;15(3). pii: E74. doi: 10.3390/md15030074. <a href="https://doi.org/10.3390/md15030074">Link to article on publisher's site</a>
dc.identifier.issn1660-3397 (Linking)
dc.identifier.doi10.3390/md15030074
dc.identifier.pmid28294970
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40315
dc.description.abstractBACKGROUND: Parenteral nutrition is often a mandatory therapeutic strategy for cases of septicemia. Likewise, therapeutic application of anti-oxidants, anti-inflammatory therapy, and endotoxin lowering, by removal or inactivation, might be beneficial to ameliorate the systemic inflammatory response during the acute phases of critical illness. Concerning anti-inflammatory properties in this setting, omega-3 fatty acids of marine origin have been frequently described. This study investigated the anti-inflammatory and LPS-inactivating properties of krill oil (KO)-in-water emulsion in human macrophages in vitro. MATERIALS AND METHODS: Differentiated THP-1 macrophages were activated using specific ultrapure-LPS that binds only on the toll-like receptor 4 (TLR4) in order to determine the inhibitory properties of the KO emulsion on the LPS-binding capacity, and the subsequent release of TNF-alpha. RESULTS: KO emulsion inhibited the macrophage binding of LPS to the TLR4 by 50% (at 12.5 microg/mL) and 75% (at 25 microg/mL), whereas, at 50 microg/mL, completely abolished the LPS binding. Moreover, KO (12.5 microg/mL, 25 microg/mL, or 50 microg/mL) also inhibited (30%, 40%, or 75%, respectively) the TNF-alpha release after activation with 0.01 microg/mL LPS in comparison with LPS treatment alone. CONCLUSION: KO emulsion influences the LPS-induced pro-inflammatory activation of macrophages, possibly due to inactivation of the LPS binding capacity.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28294970&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2017 by the authors.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectLPS
dc.subjectcytokines
dc.subjectkrill oil-in-water emulsion
dc.subjectomega-3 fatty acids
dc.subjectphospholipids
dc.subjectseptic shock
dc.subjectChemicals and Drugs
dc.subjectMedicinal Chemistry and Pharmaceutics
dc.subjectPharmacy and Pharmaceutical Sciences
dc.titleKrill Oil-In-Water Emulsion Protects against Lipopolysaccharide-Induced Proinflammatory Activation of Macrophages In Vitro
dc.typeJournal Article
dc.source.journaltitleMarine drugs
dc.source.volume15
dc.source.issue3
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4122&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3116
dc.identifier.contextkey10737547
refterms.dateFOA2022-08-23T16:43:32Z
html.description.abstract<p>BACKGROUND: Parenteral nutrition is often a mandatory therapeutic strategy for cases of septicemia. Likewise, therapeutic application of anti-oxidants, anti-inflammatory therapy, and endotoxin lowering, by removal or inactivation, might be beneficial to ameliorate the systemic inflammatory response during the acute phases of critical illness. Concerning anti-inflammatory properties in this setting, omega-3 fatty acids of marine origin have been frequently described. This study investigated the anti-inflammatory and LPS-inactivating properties of krill oil (KO)-in-water emulsion in human macrophages in vitro.</p> <p>MATERIALS AND METHODS: Differentiated THP-1 macrophages were activated using specific ultrapure-LPS that binds only on the toll-like receptor 4 (TLR4) in order to determine the inhibitory properties of the KO emulsion on the LPS-binding capacity, and the subsequent release of TNF-alpha.</p> <p>RESULTS: KO emulsion inhibited the macrophage binding of LPS to the TLR4 by 50% (at 12.5 microg/mL) and 75% (at 25 microg/mL), whereas, at 50 microg/mL, completely abolished the LPS binding. Moreover, KO (12.5 microg/mL, 25 microg/mL, or 50 microg/mL) also inhibited (30%, 40%, or 75%, respectively) the TNF-alpha release after activation with 0.01 microg/mL LPS in comparison with LPS treatment alone.</p> <p>CONCLUSION: KO emulsion influences the LPS-induced pro-inflammatory activation of macrophages, possibly due to inactivation of the LPS binding capacity.</p>
dc.identifier.submissionpathoapubs/3116
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pages74


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