High-intensity interval training attenuates development of autoimmune encephalomyelitis solely by systemic immunomodulation

Yehuda Goldberg, Shir Segal, Liel Hamdi, Hanan Nabat, Nina Fainstein, Efrat Mediouni, Yarden Asis, Paschalis Theotokis, Ilias Salamotas, Nikolaos Grigoriadis, Abram Katz, Tamir Ben-Hur, Ofira Einstein

Research output: Contribution to journalArticlepeer-review


The impact of high-intensity interval training (HIIT) on the central nervous system (CNS) in autoimmune neuroinflammation is not known. The aim of this study was to determine the direct effects of HIIT on the CNS and development of experimental autoimmune encephalomyelitis (EAE). Healthy mice were subjected to HIIT by treadmill running and the proteolipid protein (PLP) transfer EAE model was utilized. To examine neuroprotection, PLP-reactive lymph-node cells (LNCs) were transferred to HIIT and sedentary (SED) mice. To examine immunomodulation, PLP-reactive LNCs from HIIT and SED donor mice were transferred to naïve recipients and analyzed in vitro. HIIT in recipient mice did not affect the development of EAE following exposure to PLP-reactive LNCs. HIIT mice exhibited enhanced migration of systemic autoimmune cells into the CNS and increased demyelination. In contrast, EAE severity in recipient mice injected with PLP-reactive LNCs from HIIT donor mice was significantly diminished. The latter positive effect was associated with decreased migration of autoimmune cells into the CNS and inhibition of very late antigen (VLA)-4 expression in LNCs. Thus, the beneficial effect of HIIT on EAE development is attributed solely to systemic immunomodulatory effects, likely because of systemic inhibition of autoreactive cell migration and reduced VLA-4 integrin expression.

Original languageEnglish
Article number16513
JournalScientific Reports
Issue number1
StatePublished - Dec 2023

All Science Journal Classification (ASJC) codes

  • General


Dive into the research topics of 'High-intensity interval training attenuates development of autoimmune encephalomyelitis solely by systemic immunomodulation'. Together they form a unique fingerprint.

Cite this