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dc.contributor.authorAnuforo, Osk U U
dc.contributor.authorBjarnarson, Stefania P
dc.contributor.authorJonasdottir, Hulda S
dc.contributor.authorGiera, Martin
dc.contributor.authorHardardottir, Ingibjorg
dc.contributor.authorFreysdottir, Jona
dc.date.accessioned2018-02-26T15:31:53Z
dc.date.available2018-02-26T15:31:53Z
dc.date.issued2018-01
dc.date.submitted2018
dc.identifier.citationNatural killer cells play an essential role in resolution of antigen-induced inflammation in mice. 2018, 93:1-8 Mol. Immunol.en
dc.identifier.issn1872-9142
dc.identifier.pmid29112834
dc.identifier.doi10.1016/j.molimm.2017.10.019
dc.identifier.urihttp://hdl.handle.net/2336/620484
dc.descriptionTo access publisher's full text version of this article click on the hyperlink belowen
dc.description.abstractThis study examined whether NK cells are important for resolution of antigen-induced inflammation. C57BL/6 mice were immunized twice with methylated BSA (mBSA) and inflammation induced by intraperitoneal injection of mBSA. Mice were injected intravenously with anti-asialo GM1 (αASGM1) or a control antibody 24h prior to peritonitis induction and peritoneal exudate collected at different time points. Expression of surface molecules and apoptosis on peritoneal cells was determined by flow cytometry and concentration of chemokines, cytokines, soluble cytokine receptors and lipid mediators by ELISA and LC-MS/MS. Apoptosis in parathymic lymph nodes and spleens was determined by TUNEL staining. Mice administered αASGM1 had lower peritoneal NK cell numbers and a higher number of peritoneal neutrophils 12h after induction of inflammation than control mice. The number of neutrophils was still high in the αASGM1 treated mice when their number had returned to baseline levels in the control mice, 48h after induction of inflammation. Peritoneal concentrations of the neutrophil regulators G-CSF and IL-12p40 were higher at 12h in the αASGM1 treated mice than in the control mice, whereas concentrations of lipid mediators implicated in resolution of inflammation, i.e. LXA4and PGE2, were lower. Reduced apoptosis was detected in peritoneal neutrophils as well as in draining lymph nodes and spleens from the αASGM1 treated mice compared with that in the control mice. In addition, αASGM1 treated mice had lower number of peritoneal NK cells expressing NKp46 and NKG2D, receptors implicated in NK cell-induced neutrophil apoptosis. Furthermore, αASGM1 treatment completely blocked the increase in CD27+NK cells that occurred in control mice following induction of inflammation, but CD27+NK cells have been suggested to have a regulatory role. These results indicate a crucial role for NK cells in resolution of antigen-induced inflammation and suggest their importance in tempering neutrophil recruitment and maintaining neutrophil apoptosis.
dc.description.sponsorshipLandspitali University Hospital Research Fund University of Iceland Research Fund in Iceland Prof. Jan Veltkamp fonds in Netherlandsen
dc.language.isoenen
dc.publisherPergamon Elsevier Scienceen
dc.relation.urlhttps://reader.elsevier.com/reader/sd/E64C7F2BAF2E61E2F96B19D2E97FF67E8CD276D068921683BBA4C5157DE21302A20725CF6F3DAFA1826A6FF4C18594FBen
dc.rightsArchived with thanks to Molecular immunologyen
dc.subjectFrumuren
dc.subjectFrumulíffræðien
dc.subjectMótefnien
dc.subjectÓnæmisfræðien
dc.subjectNAF12en
dc.subject.meshAnimalsen
dc.subject.meshAntibodiesen
dc.subject.meshAntigensen
dc.subject.meshApoptosisen
dc.subject.meshChemokinesen
dc.subject.meshDinoprostoneen
dc.subject.meshFemaleen
dc.subject.meshG(M1) Gangliosideen
dc.subject.meshGranulocyte Colony-Stimulating Factoren
dc.subject.meshImmunophenotypingen
dc.subject.meshInflammation Mediatorsen
dc.subject.meshInterleukin-12 Subunit p40en
dc.subject.meshKiller Cells, Naturalen
dc.subject.meshLipoxinsen
dc.subject.meshLymph Nodesen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshNeutrophil Infiltrationen
dc.subject.meshPeritonitisen
dc.subject.meshReceptors, Natural Killer Cellen
dc.subject.meshSerum Albumin, Bovineen
dc.subject.meshSpleenen
dc.titleNatural killer cells play an essential role in resolution of antigen-induced inflammation in mice.en
dc.typeArticleen
dc.contributor.department[ 1 ] Univ Iceland, Biomed Ctr, Biochem & Mol Biol, Fac Med, Reykjavik, Iceland [ 2 ] Landspitali Natl Univ Hosp Iceland, Dept Immunol, Bld 14 Eiriksgata, IS-101 Reykjavik, Iceland [ 3 ] Landspitali Natl Univ Hosp Iceland, Ctr Rheumatol Res, Reykjavik, Iceland Show more [ 4 ] Univ Iceland, Dept Immunol, Biomed Ctr, Fac Med, Reykjavik, Iceland Show more [ 5 ] Leiden Univ, Ctr Prote & Metabol, Med Ctr, Leiden, Netherlandsen
dc.identifier.journalMolecular immunologyen
dc.rights.accessLandspitali Access - LSH-aðganguren
dc.departmentcodeNAF12
html.description.abstractThis study examined whether NK cells are important for resolution of antigen-induced inflammation. C57BL/6 mice were immunized twice with methylated BSA (mBSA) and inflammation induced by intraperitoneal injection of mBSA. Mice were injected intravenously with anti-asialo GM1 (αASGM1) or a control antibody 24h prior to peritonitis induction and peritoneal exudate collected at different time points. Expression of surface molecules and apoptosis on peritoneal cells was determined by flow cytometry and concentration of chemokines, cytokines, soluble cytokine receptors and lipid mediators by ELISA and LC-MS/MS. Apoptosis in parathymic lymph nodes and spleens was determined by TUNEL staining. Mice administered αASGM1 had lower peritoneal NK cell numbers and a higher number of peritoneal neutrophils 12h after induction of inflammation than control mice. The number of neutrophils was still high in the αASGM1 treated mice when their number had returned to baseline levels in the control mice, 48h after induction of inflammation. Peritoneal concentrations of the neutrophil regulators G-CSF and IL-12p40 were higher at 12h in the αASGM1 treated mice than in the control mice, whereas concentrations of lipid mediators implicated in resolution of inflammation, i.e. LXA4and PGE2, were lower. Reduced apoptosis was detected in peritoneal neutrophils as well as in draining lymph nodes and spleens from the αASGM1 treated mice compared with that in the control mice. In addition, αASGM1 treated mice had lower number of peritoneal NK cells expressing NKp46 and NKG2D, receptors implicated in NK cell-induced neutrophil apoptosis. Furthermore, αASGM1 treatment completely blocked the increase in CD27+NK cells that occurred in control mice following induction of inflammation, but CD27+NK cells have been suggested to have a regulatory role. These results indicate a crucial role for NK cells in resolution of antigen-induced inflammation and suggest their importance in tempering neutrophil recruitment and maintaining neutrophil apoptosis.


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