Forced Exercise Preconditioning Attenuates Experimental Autoimmune Neuritis by Altering Th1 Lymphocyte Composition and Egress Journal Article

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Authors: Calik, M. W.; Shankarappa, S. A.; Langert, K. A.; Stubbs, E. B., Jr
Article Title: Forced Exercise Preconditioning Attenuates Experimental Autoimmune Neuritis by Altering Th1 Lymphocyte Composition and Egress
Abstract: A short-term exposure to moderately intense physical exercise affords a novel measure of protection against autoimmune-mediated 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 x 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 = 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 ( approximately 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.
Journal Title: ASN neuro
Volume: 7
Issue: 4
ISSN: 1759-0914
Publisher: Unknown  
Journal Place: United States
Date Published: 2015
Start Page: 10.1177/1759091415595726. Print 2015 Jul
Language: eng
DOI/URL:

10.1177/1759091415595726
Notes: LR: 20150722; CI: (c) The Author(s) 2015; GR: I01 RX000130/RX/RRD VA/United States; JID: 101507115; OTO: NOTNLM; 2015/07 [ppublish]; epublish