ISD researchers hypothesized in a newly published study that the high rate of comorbidities that develop after a stroke could have a common immunological cause. A Myeloid innate immune memory was identified as causing remote organ dysfunction post-stroke. Single-cell sequencing revealed persistent pro-inflammatory changes in monocytes/macrophages up to 3 months after brain injury, especially in the heart, causing cardiac fibrosis and dysfunction. Neutralizing IL-1β or blocking monocyte trafficking prevented post-stroke cardiac dysfunction, suggesting immune-targeted therapies for secondary prevention.
Simats A, Zhang S, Messerer D, Chong F, Beşkardeş S, Chivukula AS, Cao J, Besson-Girard S, Montellano FA, Morbach C, Carofiglio O, Ricci A, Roth S, Llovera G, Singh R, Chen Y, Filser S, Plesnila N, Braun C, Spitzer H, Gokce O, Dichgans M, Heuschmann PU, Hatakeyama K, Beltrán E, Clauss S, Bonev B, Schulz C, Liesz A. Innate immune memory after brain injury drives inflammatory cardiac dysfunction. Cell. 2024 Jul 12:S0092-8674(24)00702-5. doi: 10.1016/j.cell.2024.06.028. Epub ahead of print.
