Forced Exercise.pdf (616.24 kB)
Download fileForced Exercise Preconditioning Attenuates Experimental Autoimmune Neuritis by Altering Th1 Lymphocyte Composition and Egress
journal contribution
posted on 2016-01-20, 00:00 authored by MW Calik, SA Shankarappa, KA Langert, EB Jr. StubbsA short-term exposure to moderately intense physical exercise affords a novel measure of protection against autoimmunemediated
peripheral nerve injury. Here, we investigated the mechanism by which forced exercise attenuates the development
and progression of experimental autoimmune neuritis (EAN), an established animal model of Guillain–Barre´ syndrome. Adult
male Lewis rats remained sedentary (control) or were preconditioned with forced exercise (1.2 km/day 3 weeks) prior to
P2-antigen induction of EAN. Sedentary rats developed a monophasic course of EAN beginning on postimmunization day
12.3 0.2 and reaching peak severity on day 17.0 0.3 (N ¼ 12). By comparison, forced-exercise preconditioned rats
exhibited a similar monophasic course but with significant (p <.05) reduction of disease severity. Analysis of popliteal
lymph nodes revealed a protective effect of exercise preconditioning on leukocyte composition and egress. Compared
with sedentary controls, forced exercise preconditioning promoted a sustained twofold retention of P2-antigen responsive
leukocytes. The percentage distribution of pro-inflammatory (Th1) lymphocytes retained in the nodes from sedentary EAN
rats (5.1 0.9%) was significantly greater than that present in nodes from forced-exercise preconditioned EAN rats
(2.9 0.6%) or from adjuvant controls (2.0 0.3%). In contrast, the percentage of anti-inflammatory (Th2) lymphocytes
(7–10%) and that of cytotoxic T lymphocytes ( 20%) remained unaltered by forced exercise preconditioning. These data do
not support an exercise-inducible shift in Th1:Th2 cell bias. Rather, preconditioning with forced exercise elicits a sustained
attenuation of EAN severity, in part, by altering the composition and egress of autoreactive proinflammatory (Th1) lymphocytes
from draining lymph nodes.
Keyw