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dc.contributor.author Tímár Csaba
dc.contributor.author Lőrincz Márton Ákos
dc.contributor.author Csépányi-Kömi Roland
dc.contributor.author Valyi-Nagy Anna
dc.contributor.author Nagy György
dc.contributor.author Buzás Edit Irén
dc.contributor.author Iványi Zsolt
dc.contributor.author Kittel Ágnes
dc.contributor.author David W. Powell
dc.contributor.author Kenneth R. McLeish
dc.contributor.author Ligeti Erzsébet
dc.date.accessioned 2015-12-07T08:00:27Z
dc.date.available 2015-12-07T08:00:27Z
dc.date.issued 2013
dc.identifier 84872469459
dc.identifier.citation pagination=510-518; journalVolume=121; journalIssueNumber=3; journalTitle=BLOOD;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/2650
dc.identifier.uri doi:10.1182/blood-2012-05-431114
dc.description.abstract Cell-derived vesicles represent a recently discovered mechanism for intercellular communication. We investigated their potential role in interaction of microbes with host organisms. We provide evidence that different stimuli induced isolated neutrophilic granulocytes to release microvesicles with different biologic properties. Only opsonized particles initiated the formation of microvesicles that were able to impair bacterial growth. The antibacterial effect of neutrophil-derived microvesicles was independent of production of toxic oxygen metabolites and opsonization or engulfment of the microbes, but depended on β(2) integrin function, continuous actin remodeling, and on the glucose supply. Neutrophil-derived microvesicles were detected in the serum of healthy donors, and their number was significantly increased in the serum of bacteremic patients. We propose a new extracellular mechanism to restrict bacterial growth and dissemination.
dc.relation.ispartof urn:issn:0006-4971
dc.title Antibacterial effect of microvesicles released from human neutrophilic granulocytes
dc.type Journal Article
dc.date.updated 2015-11-24T12:58:54Z
dc.language.rfc3066 en
dc.identifier.mtmt 2114488
dc.identifier.wos 000313727500015
dc.identifier.pubmed 23144171
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.department SE/AOK/I/Genetikai, Sejt- és Immunbiológiai Intézet
dc.contributor.department SE/AOK/K/Aneszteziológiai és Intenzív Terápiás Klinika
dc.contributor.institution Semmelweis Egyetem
dc.mtmt.swordnote Timar CI and Lorincz AM contributed equally to this work


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