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dc.contributor.authorThorburn, Taylor
dc.date.accessioned2019-10-04T11:44:01Z
dc.date.available2019-10-04T11:44:01Z
dc.identifier.urihttp://hdl.handle.net/10222/76431
dc.description.abstractSepsis is characterized by a dysregulated immune response to infection, causing damage to tissues and organs. As part of the inflammatory response, iron catalyzes the generation of reactive oxygen species (ROS). In the present study, we sought to evaluate the anti-inflammatory effects of a novel iron chelator, DIBI, in vitro and in two murine models of sepsis in vivo. In vitro, we found that DIBI reduced ROS production by innate immune cells. In vivo immune cell activation was evaluated in the intestinal microcirculation using intravital microscopy. In both sepsis models, anti-inflammatory actions were observed upon administration of DIBI, whereby DIBI reduced sepsis-induced leukocyte adhesion and preserved capillary perfusion in the intestinal microvasculature. Therefore, our data presents a promising role for iron chelation as a therapeutic option for sepsis, in which DIBI reduces ROS generation by binding iron.en_US
dc.language.isoenen_US
dc.subjectmicrocirculationen_US
dc.subjectIntravital microscopyen_US
dc.subjectinnate immunityen_US
dc.subjectsepsisen_US
dc.subjectironen_US
dc.subjectinflammationen_US
dc.subjectchelationen_US
dc.subjectreactive oxygen speciesen_US
dc.titleIron-related immune cell function in sepsisen_US
dc.date.defence2018-07-25
dc.contributor.departmentDepartment of Microbiology & Immunologyen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.external-examinerDr. Orlando Hungen_US
dc.contributor.graduate-coordinatorDr. Brent Johnstonen_US
dc.contributor.thesis-readerDr. Andrew Stadnyken_US
dc.contributor.thesis-readerDr. Bruce Holbeinen_US
dc.contributor.thesis-supervisorDr. David Hoskinen_US
dc.contributor.thesis-supervisorDr. Christian Lehmannen_US
dc.contributor.ethics-approvalReceiveden_US
dc.contributor.manuscriptsNot Applicableen_US
dc.contributor.copyright-releaseNoen_US
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