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Phospholipase C activator m-3M3FBS protects against morbidity and mortality associated with sepsis

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dc.contributor.authorKim, SD-
dc.contributor.authorKim, HJ-
dc.contributor.authorShim, JW-
dc.contributor.authorLee, HY-
dc.contributor.authorLee, SK-
dc.contributor.authorKwon, S-
dc.contributor.authorJung, YS-
dc.contributor.authorBaek, SH-
dc.contributor.authorPark, JS-
dc.contributor.authorZabel, BA-
dc.contributor.authorBae, YS-
dc.date.accessioned2013-04-23T01:52:15Z-
dc.date.available2013-04-23T01:52:15Z-
dc.date.issued2012-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/7848-
dc.description.abstractAlthough phospholipase C (PLC) is a crucial enzyme required for effective signal transduction and leukocyte activation, the role of PLC in polymicrobial sepsis remains unclear. In this study, we show that the direct PLC activator m-3M3FBS treatment significantly attenuates vital organ inflammation, widespread immune cell apoptosis, and mortality in a mouse sepsis model induced by lethal cecal ligation and puncture challenge. Mechanistically, m-3M3FBS-dependent protection was largely abolished by pretreatment of mice with the PLC-selective inhibitor U-73122, thus confirming PLC agonism by m-3M3FBS in vivo. PLC activation enhanced the bactericidal activity and hydrogen peroxide production of mouse neutrophils, and it also enhanced the production of IFN-γ and IL-12 while inhibiting proseptic TNF-α and IL-1β production in cecal ligation and puncture mice. In a second model of sepsis, PLC activation also inhibited the production of TNF-α and IL-1β following systemic LPS challenge. In conclusion, we show that agonizing the central signal transducing enzyme PLC by m-3M3FBS can reverse the progression of toxic shock by triggering multiple protective downstream signaling pathways to maintain organ function, leukocyte survival, and to enhance microbial killing.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis-
dc.subject.MESHCytokines-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHIn Situ Nick-End Labeling-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred ICR-
dc.subject.MESHNeutrophils-
dc.subject.MESHSepsis-
dc.subject.MESHSulfonamides-
dc.subject.MESHType C Phospholipases-
dc.titlePhospholipase C activator m-3M3FBS protects against morbidity and mortality associated with sepsis-
dc.typeArticle-
dc.identifier.pmid22798676-
dc.identifier.urlhttp://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=22798676-
dc.contributor.affiliatedAuthor박, 준성-
dc.type.localJournal Papers-
dc.identifier.doi10.4049/jimmunol.1200635-
dc.citation.titleJournal of immunology (Baltimore, Md. : 1950)-
dc.citation.volume189-
dc.citation.number4-
dc.citation.date2012-
dc.citation.startPage2000-
dc.citation.endPage2005-
dc.identifier.bibliographicCitationJournal of immunology (Baltimore, Md. : 1950), 189(4). : 2000-2005, 2012-
dc.identifier.eissn1550-6606-
dc.relation.journalidJ000221767-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Hematology-Oncology
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