No evidence of progressive proinflammatory cytokine storm in brain-dead organ donors - A time-course analysis using clinical samples
dc.contributor.author | Bera, KD | |
dc.contributor.author | Tabak, J | |
dc.contributor.author | Ploeg, RJ | |
dc.date.accessioned | 2024-01-10T13:34:15Z | |
dc.date.issued | 2024-01-09 | |
dc.date.updated | 2024-01-09T18:42:08Z | |
dc.description.abstract | Background. Solid organ transplantation is a cost-effective treatment for end-stage organ failure. Organ donation after brain death is an important source of transplanted organs. Data are limited on the effects of brain injury or donor management on grafts. The consensus view has been that brain death creates a progressively proinflammatory environment. We aimed to investigate time-course changes across a range of cytokines in a donation after brain death cohort of donors who died of intracranial hemorrhage without any other systemic source of inflammation. Methods. A donor cohort was defined using the UK Quality in Organ Donation biobank. Serum levels of proteins involved in proinflammatory and brain injury pathways (tumor necrosis factor-alpha, interleukin-6, complement C5a, neuron-specific enolase, and glial fibrillary acidic protein) were measured from admission to organ recovery. Moving median analysis was used to combine donor trajectories and delineate a time-course. Results. A cohort of 27 donors with brain death duration between 10 and 30h was created, with 24 donors contributing to the time-course analysis. We observed no increase in tumor necrosis factor-alpha or interleukin-6 throughout the donor management period. Neuronal injury marker and complement C5a remain high from admission to organ recovery, whereas glial fibrillary acidic protein rises around the confirmation of brain death. Conclusions. We found no evidence of a progressive rise of proinflammatory mediators with prolonged duration of brain death, questioning the hypothesis of a progressively proinflammatory environment. Furthermore, the proposed approach allows us to study chronological changes and identify biomarkers or target pathways when logistical or ethical considerations limit sample availability. | en_GB |
dc.description.sponsorship | Oxford Transplant Foundation | en_GB |
dc.description.sponsorship | National Institute for Health and Care Research (NIHR) | en_GB |
dc.identifier.citation | Published online 9 January 2024 | en_GB |
dc.identifier.doi | 10.1097/TP.0000000000004900 | |
dc.identifier.grantnumber | R56956/AA001 | en_GB |
dc.identifier.uri | http://hdl.handle.net/10871/134973 | |
dc.identifier | ORCID: 0000-0002-0588-957X (Tabak-Sznajder, Joel) | |
dc.language.iso | en | en_GB |
dc.publisher | Wolters Kluwer Health, Inc. | en_GB |
dc.rights | © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. | en_GB |
dc.title | No evidence of progressive proinflammatory cytokine storm in brain-dead organ donors - A time-course analysis using clinical samples | en_GB |
dc.type | Article | en_GB |
dc.date.available | 2024-01-10T13:34:15Z | |
dc.identifier.issn | 1534-6080 | |
dc.description | This is the final version. Available on open access from Wolters Kluwer Health via the DOI in this record. | en_GB |
dc.identifier.journal | Transplantation | en_GB |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | en_GB |
dcterms.dateAccepted | 2023-10-25 | |
dcterms.dateSubmitted | 2023-05-15 | |
rioxxterms.version | VoR | en_GB |
rioxxterms.licenseref.startdate | 2023-10-25 | |
rioxxterms.type | Journal Article/Review | en_GB |
refterms.dateFCD | 2024-01-10T13:28:28Z | |
refterms.versionFCD | VoR | |
refterms.dateFOA | 2024-01-10T13:34:19Z | |
refterms.panel | A | en_GB |
refterms.dateFirstOnline | 2024-01-09 |
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is an open access article distributed under the Creative Commons Attribution
License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.