Nature communications · 2025
Exercise facilitates post-stroke recovery through mitigation of neuronal hyperexcitability via interleukin-10 signaling.
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Schmidt-Pogoda A, Ruck T, Strecker J K, Hoppen M, Fazio L, Vinnenberg L, Maus B, Wachsmuth L, Cerina M, Diederich K, Lichtenberg S, Abberger H, Haertel Lal, Schafflick D, Meyer Zu Hörste G, Herrmann A M, Hundehege P, Narayanan V, Nelke C, Kruithoff K, Bosbach J, Vicari E, Ramcke T, Beuker C, Hadaschik E, Budde T, Faber C, Wiendl H, Hansen W, Meuth S G, Minnerup J
Аннотация
Physical exercise is an effective therapy for improving stroke recovery. However, the exact underlying molecular mechanisms of exercise-enhanced neuronal repair remain unclear. As exercise affects the immune system in healthy individuals, and the immune system in turn influences recovery after stroke, we hypothesized that immune mechanisms play a role in exercise-induced neurological recovery. Using a model of ischemic stroke in adult male mice, we here show that the presence of regulatory T cells (Treg) within the ischemic brain is a prerequisite for exercise-enhanced functional and structural recovery. Treg prevent excessive and sustained hyperexcitability of periinfarct neurons via IL-10 signaling. This reduced hyperexcitability precedes alterations in neuronal connectivity, which underlie functional improvement. Together, we delineate the interaction of exercise-therapy, the immune system and functional recovery after ischemic stroke. Our findings can have translational relevance for further development of immune-targeted therapies.