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

Barone, Damiano G.; Carnicer-Lombarte, Alejandro; Tourlomousis, Panagiotis; Hamilton, Russell S.; Prater, Malwina; Rutz, Alexandra L.; Dimov, Ivan B.; Malliaras, George G.; Lacour, Stephanie P.; Robertson, Avril A. B.; Franze, Kristian; Fawcett, James W.; Bryant, Clare E.

doi:10.1073/pnas.2115857119

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

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Franze, Kristian
Abteilung Franze, Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;
Friedrich-Alexander-Universität Erlangen-Nürnberg, External Organizations;

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Citation

Barone, D. G., Carnicer-Lombarte, A., Tourlomousis, P., Hamilton, R. S., Prater, M., Rutz, A. L., et al. (2022). Prevention of the foreign body response to implantable medical devices by inflammasome inhibition. Proceedings of the National Academy of Sciences of the United States of America, 119(12), e2115857119. doi:10.1073/pnas.2115857119.

Cite as: https://hdl.handle.net/21.11116/0000-000F-8719-D

Abstract

SignificanceImplantable 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.