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dc.contributor.authorChristaki, Eirinien
dc.contributor.authorDiza, Evdoxiaen
dc.contributor.authorGiamarellos-Bourboulis, Evangelos J.en
dc.contributor.authorPapadopoulou, Nikolettaen
dc.contributor.authorPistiki, Aikaterinien
dc.contributor.authorDroggiti, Dionysia-Irinien
dc.contributor.authorGeorgitsi, Mariannaen
dc.contributor.authorMachova, Alzbetaen
dc.contributor.authorLambrelli, Dimitraen
dc.contributor.authorMalisiovas, Nicolaosen
dc.contributor.authorNikolaidis, Pavlosen
dc.contributor.authorOpal, Steven M.en
dc.creatorChristaki, Eirinien
dc.creatorDiza, Evdoxiaen
dc.creatorGiamarellos-Bourboulis, Evangelos J.en
dc.creatorPapadopoulou, Nikolettaen
dc.creatorPistiki, Aikaterinien
dc.creatorDroggiti, Dionysia-Irinien
dc.creatorGeorgitsi, Mariannaen
dc.creatorMachova, Alzbetaen
dc.creatorLambrelli, Dimitraen
dc.creatorMalisiovas, Nicolaosen
dc.creatorNikolaidis, Pavlosen
dc.creatorOpal, Steven M.en
dc.description.abstractBackground. Natural killer (NK) and natural killer T (NKT) cells contribute to the innate host defense but their role in bacterial sepsis remains controversial. Methods. C57BL/6 mice were infected intratracheally with 5 x 10(5) cfu of Streptococcus pneumoniae. Animals were divided into sham group (Sham); pretreated with isotype control antibody (CON) group; pretreated with anti-asialo GM1 antibody (NKd) group; and pretreated with anti-CD1d monoclonal antibody (NKTd) group before bacterial challenge. Serum and tissue samples were analyzed for bacterial load, cytokine levels, splenocyte apoptosis rates, and cell characteristics by flow cytometry. Splenocyte miRNA expression was also analyzed and survival was assessed. Results. NK cell depletion prolonged survival. Upon inhibition of NKTcell activation, spleen NK(CD3-/NK1.1+) cells increased compared to all other groups. Inhibition of NKT cell activation led to higher bacterial loads and increased levels of serum and splenocyte IFN-gamma. Splenocyte miRNA analysis showed that miR-200c and miR-29a were downregulated, while miR-125a-5p was upregulated, in anti-CD1d treated animals. These changes were moderate after NK cell depletion. Conclusions. NK cells appear to contribute to mortality in pneumococcal pneumonia. Inhibition of NKT cell activation resulted in an increase in spleen NK (CD3-/NK1.1+) cells and a higher IFN-gamma production, while altering splenocyte miRNA expression.en
dc.sourceJournal of Immunology Researchen
dc.titleNK and NKT Cell Depletion Alters the Outcome of Experimental Pneumococcal Pneumonia: Relationship with Regulation of Interferon-gamma Productionen
dc.identifier.doi10.1155/2015/532717Ιατρική Σχολή / Medical School
dc.contributor.orcidChristaki, Eirini [0000-0002-8152-6367]
dc.contributor.orcidGiamarellos-Bourboulis, Evangelos J. [0000-0003-4713-3911]
dc.contributor.orcidGeorgitsi, Marianna [0000-0002-0354-0913]

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