Christaki, Eirini ORCID: 0000-0002-8152-6367, Diza, Evdoxia, Giamarellos-Bourboulis, Evangelos J., Papadopoulou, Nikoletta, Pistiki, Aikaterini, Droggiti, Dionysia-Irini, Georgitsi, Marianna, Machova, Alzbeta, Lambrelli, Dimitra, Malisiovas, Nicolaos, Nikolaidis, Pavlos and Opal, Steven M. (2015). NK and NKT Cell Depletion Alters the Outcome of Experimental Pneumococcal Pneumonia: Relationship with Regulation of Interferon-gamma Production. J Immunol. Res., 2015. LONDON: HINDAWI LTD. ISSN 2314-7156

Full text not available from this repository.

Abstract

Background. 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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Christaki, EiriniUNSPECIFIEDorcid.org/0000-0002-8152-6367UNSPECIFIED
Diza, EvdoxiaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Giamarellos-Bourboulis, Evangelos J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Papadopoulou, NikolettaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Pistiki, AikateriniUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Droggiti, Dionysia-IriniUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Georgitsi, MariannaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Machova, AlzbetaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Lambrelli, DimitraUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Malisiovas, NicolaosUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Nikolaidis, PavlosUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Opal, Steven M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-416424
DOI: 10.1155/2015/532717
Journal or Publication Title: J Immunol. Res.
Volume: 2015
Date: 2015
Publisher: HINDAWI LTD
Place of Publication: LONDON
ISSN: 2314-7156
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
NATURAL-KILLER-CELLS; T-CELLS; CD1D-INDEPENDENT ACTIVATION; INFLAMMATORY RESPONSES; GLYCOLIPID ANTIGENS; MICRORNA REGULATION; UNITED-STATES; CUTTING EDGE; INNATE; SEPSISMultiple languages
ImmunologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/41642

Downloads

Downloads per month over past year

Altmetric

Export

Actions (login required)

View Item View Item