Stroke induces disease-specific myeloid cells in the brain parenchyma and pia

Carolin Beuker, David Schafflick, Jan-Kolja Strecker, Michael Heming, Xiaolin Li, Jolien Wolbert, Antje Schmidt-Pogoda, Christian Thomas, Tanja Kuhlmann, Irene Aranda-Pardos, Noelia A-Gonzalez, Praveen Ashok Kumar, Yves Werner, Ertugrul Kilic, Dirk M. Hermann, Heinz Wiendl, Ralf Stumm, Gerd Meyer zu Hörste () and Jens Minnerup ()
Additional contact information
Carolin Beuker: University Hospital
David Schafflick: University Hospital
Jan-Kolja Strecker: University Hospital
Michael Heming: University Hospital
Xiaolin Li: University Hospital
Jolien Wolbert: University Hospital
Antje Schmidt-Pogoda: University Hospital
Christian Thomas: University of Münster
Tanja Kuhlmann: University of Münster
Irene Aranda-Pardos: Westfälische Wilhelms-University
Noelia A-Gonzalez: Westfälische Wilhelms-University
Praveen Ashok Kumar: Jena University Hospital
Yves Werner: Jena University Hospital
Ertugrul Kilic: Istanbul Medipol University Regenerative and Restorative Medical Research Center
Dirk M. Hermann: University Hospital Essen
Heinz Wiendl: University Hospital
Ralf Stumm: Jena University Hospital
Gerd Meyer zu Hörste: University Hospital
Jens Minnerup: University Hospital

Nature Communications, 2022, vol. 13, issue 1, 1-14

Abstract: Abstract Inflammation triggers secondary brain damage after stroke. The meninges and other CNS border compartments serve as invasion sites for leukocyte influx into the brain thus promoting tissue damage after stroke. However, the post-ischemic immune response of border compartments compared to brain parenchyma remains poorly characterized. Here, we deeply characterize tissue-resident leukocytes in meninges and brain parenchyma and discover that leukocytes respond differently to stroke depending on their site of residence. We thereby discover a unique phenotype of myeloid cells exclusive to the brain after stroke. These stroke-associated myeloid cells partially resemble neurodegenerative disease-associated microglia. They are mainly of resident microglial origin, partially conserved in humans and exhibit a lipid-phagocytosing phenotype. Blocking markers specific for these cells partially ameliorates stroke outcome thus providing a potential therapeutic target. The injury-response of myeloid cells in the CNS is thus compartmentalized, adjusted to the type of injury and may represent a therapeutic target.

Date: 2022
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DOI: 10.1038/s41467-022-28593-1

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