Exercise intensity‐dependent immunomodulatory effects on encephalomyelitis

Abstract

Abstract Background Exercise training (ET) has beneficial effects on multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the intensity‐dependent effects of ET on the systemic immune system in EAE remain undefined. Objective (1) To compare the systemic immune modulatory effects of moderate versus high‐intensity ET protocols in protecting against development of EAE; (2) To investigate whether ET affects autoimmunity selectively, or causes general immunosuppression. Methods Healthy mice performed moderate or high‐intensity treadmill running programs. Proteolipid protein (PLP)‐induced transfer EAE was utilized to examine ET effects specifically on the systemic immune system. Lymph node (LN)‐T cells from trained versus sedentary donor mice were transferred to naïve recipients and EAE severity was assessed, by clinical assessment and histopathological analysis. LN‐T cells derived from donor trained versus sedentary PLP‐immunized mice were analyzed in vitro for proliferation assays by flow cytometry analysis and cytokine and chemokine receptor gene expression using real‐time PCR. T cell‐dependent immune responses of trained versus sedentary mice to the nonautoantigen ovalbumin and susceptibility to Escherichia coli‐induced acute peritonitis were examined. Results High‐intensity training in healthy donor mice induced significantly greater inhibition than moderate‐intensity training on proliferation and generation of encephalitogenic T cells in response to PLP‐immunization, and on EAE severity upon their transfer into recipient mice. High‐intensity training also inhibited LN‐T cell proliferation in response to ovalbumin immunization. E. coli bacterial counts and dissemination were not affected by training. Interpretation High‐intensity training induces superior effects in preventing autoimmunity in EAE, but does not alter immune responses to E. coli infection.