Interleukin-10 limits intense acute swimming-induced muscle mechanical hyperalgesia in mice.

Abstract

NEW FINDINGS:

What is the central question of this study? This study investigated the role of the endogenous anti-inflammatory cytokine interleukin-10 in intense acute swimming-induced muscle mechanical hyperalgesia in mice. What is the main finding and its importance? Endogenous interleukin-10 has a key role in limiting exercise-induced muscle pain in a model presenting similarities to delayed-onset muscle soreness in mice. Interleukin-10 reduced muscle pain by diminishing leucocyte recruitment, hyperalgesic cytokine production, oxidative stress and myocyte damage. Interleukin-10 (IL-10) is an antihyperalgesic cytokine. In this study, IL-10-deficient (IL-10(-/-) ) mice were used to investigate the role of endogenous IL-10 in intense acute swimming-induced muscle mechanical hyperalgesia, which presents similarities with delayed-onset muscle soreness. An intense acute swimming session of 1 or 2 h induced significant muscle mechanical hyperalgesia in a time-dependent manner in wild-type mice compared with the sham group 24 h after the session, which was further increased in IL-10(-/-) mice (P ˂ 0.05). Intraperitoneal treatment of wild-type mice with IL-10 (1-10 ng) reduced muscle mechanical hyperalgesia in a dose-dependent manner and reversed the enhanced muscle hyperalgesia in IL-10(-/-) mice (P ˂ 0.05). The 2 h swimming session induced increases in tumour necrosis factor-α, interleukin-1β and IL-10 production in the soleus muscle. However, tumour necrosis factor-α and interleukin-1β production in the soleus muscle were even higher in IL-10(-/-) mice between 2 and 6 h after the stimulus (P ˂ 0.05). There was no statistical difference in the levels of the antihyperalgesic cytokines interleukin-4, interleukin-5, interleukin-13 and transforming growth factor-β between wild-type and IL-10(-/-) mice (P ˃ 0.05). Interleukin-10 deficiency also resulted in increased myeloperoxidase activity, greater depletion of reduced glutathione levels, increased superoxide anion production and the maintenance of high plasma concentrations of creatine kinase (until 24 h after the swimming session) in soleus muscle (P ˂ 0.05). These results demonstrate that endogenous IL-10 controls intense acute swimming-induced muscle mechanical hyperalgesia by limiting oxidative stress and cytokine production.

• Authors: Sergio M Borghi, Felipe A Pinho-Ribeiro, Ana C Zarpelon, Thiago M Cunha, Jose C Alves-Filho, Sergio H Ferreira, Fernando Q Cunha, Rubia Casagrande, Waldiceu A Verri Jr
• Journal: Experimental physiology (Exp Physiol) Vol. 100 Issue 5 Pg. 531-44 (Apr 20 2015) ISSN: 1469-445X [Electronic] England
• PMID: 25711612 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2015 The Authors. Experimental Physiology © 2015 The Physiological Society.

Chemical References

• IL10 protein, mouse
• Interleukin-10

Topics

• Animals
• Hyperalgesia (chemically induced, metabolism)
• Inflammation (metabolism)
• Interleukin-10 (genetics, metabolism)
• Male
• Mice, Inbred C57BL
• Muscle Cells (cytology)
• Muscle, Skeletal (physiopathology)
• Myalgia (chemically induced)
• Oxidative Stress (physiology)
• Swimming