Prevention of the foreign body response to implantable medical devices by inflammasome inhibition.

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dc.contributor.authorBarone, Damiano G
dc.contributor.authorCarnicer-Lombarte, Alejandro
dc.contributor.authorTourlomousis, Panagiotis
dc.contributor.authorHamilton, Russell S
dc.contributor.authorPrater, Malwina
dc.contributor.authorRutz, Alexandra L
dc.contributor.authorDimov, Ivan B
dc.contributor.authorMalliaras, George G
dc.contributor.authorLacour, Stephanie P
dc.contributor.authorRobertson, Avril AB
dc.contributor.authorFranze, Kristian
dc.contributor.authorFawcett, James W
dc.contributor.authorBryant, Clare E
dc.date.accessioned2022-04-19T13:16:51Z
dc.date.available2022-04-19T13:16:51Z
dc.date.issued2022-03-22
dc.identifier.issn0027-8424
dc.identifier.other35298334
dc.identifier.otherPMC8944905
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/336153
dc.description.abstractSignificanceImplantable electronic medical devices (IEMDs) are used for some clinical applications, representing an exciting prospect for the transformative treatment of intractable conditions such Parkinson's disease, deafness, and paralysis. The use of IEMDs is limited at the moment because, over time, a foreign body reaction (FBR) develops at the device-neural interface such that ultimately the IEMD fails and needs to be removed. Here, we show that macrophage nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activity drives the FBR in a nerve injury model yet integration of an NLRP3 inhibitor into the device prevents FBR while allowing full healing of damaged neural tissue to occur.
dc.description.sponsorshipPart of the RNA-Seq work was performed with the Genomics and Transcriptomics Core, which is funded by the UK Medical Research Council (MRC) Metabolic Disease Unit (MRC_MC_UU_00014/5) and a Wellcome Trust Major Award (208363/Z/17/Z), and guidance from Marcella Ma, whom the authors wish to thank. CEB was supported by a Wellcome Trust Investigator award (108045/Z/15/Z). This work was also supported by the UK Wellcome Trust (Translational Medicine and Therapeutics PhD Programme Fellowship 109511/Z/15/Z to DGB), the UK Health Education England and the National Institute for Health Research (HEE/ NIHR ICA Program Clinical Lectureship CL-2019-14-004 to DGB), the UK Medical Research Council (MRC) and the Sackler Foundation (doctoral training grant RG70550 to ACL), the Engineering and Physical Sciences Research Council (EPSRC) Cambridge NanoDTC (EP/L015978/1), the Centre for Trophoblast Research (MP and RSH), the Whitaker International Scholars Program (ALR), the European Commission’s Horizon 2020 (Marie Sklodowska-Curie Fellowship 797506 to ALR), the Bertarelli Foundation (SPL), the European Research Council (Consolidator Award 772426 to KF), the UK Biotechnology and Biological Sciences Research Council (Research Grant BB/N006402/1 to KF), and the Alexander von Humboldt Foundation (Humboldt Professorship to KF).
dc.languageeng
dc.publisherProceedings of the National Academy of Sciences
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourcenlmid: 7505876
dc.sourceessn: 1091-6490
dc.subjectMCC950
dc.subjectNLRP3 inflammasome
dc.subjectforeign body reaction
dc.subjectneural interfaces
dc.subjectForeign Bodies
dc.subjectHumans
dc.subjectInflammasomes
dc.subjectMacrophages
dc.subjectNLR Family, Pyrin Domain-Containing 3 Protein
dc.subjectProstheses and Implants
dc.titlePrevention of the foreign body response to implantable medical devices by inflammasome inhibition.
dc.typeArticle
dc.date.updated2022-04-19T13:16:50Z
prism.issueIdentifier12
prism.publicationNameProc Natl Acad Sci U S A
prism.volume119
dc.identifier.doi10.17863/CAM.83578
dcterms.dateAccepted2022-01-13
rioxxterms.versionofrecord10.1073/pnas.2115857119
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidBarone, Damiano G [0000-0002-0091-385X]
dc.contributor.orcidHamilton, Russell S [0000-0002-0598-3793]
dc.contributor.orcidPrater, Malwina [0000-0002-8202-5345]
dc.contributor.orcidMalliaras, George G [0000-0002-4582-8501]
dc.contributor.orcidLacour, Stephanie P [0000-0001-9075-4022]
dc.contributor.orcidRobertson, Avril AB [0000-0002-9652-8357]
dc.contributor.orcidFranze, Kristian [0000-0002-8425-7297]
dc.contributor.orcidBryant, Clare E [0000-0002-2924-0038]
dc.identifier.eissn1091-6490
pubs.funder-project-idWellcome Trust (085686/Z/08/A)
pubs.funder-project-idEngineering and Physical Sciences Research Council (EP/L015978/1)
pubs.funder-project-idWellcome Trust (108045/Z/15/Z)
pubs.funder-project-idBiotechnology and Biological Sciences Research Council (BB/N006402/1)
pubs.funder-project-idWellcome Trust (208363/Z/17/Z)
pubs.funder-project-idEuropean Research Council (772426)
pubs.funder-project-idEuropean Commission Horizon 2020 (H2020) Marie Sk?odowska-Curie actions (797506)
pubs.funder-project-idMRC (MC_UU_00014/5)
cam.issuedOnline2022-03-17


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International