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Am J Physiol Regul Integr Comp Physiol 275: R1983-R1991, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 6, R1983-R1991, December 1998

Sepsis in mice stimulates muscle proteolysis in the absence of IL-6

Arthur Williams, Jing Jing Wang, Li Wang, Xiaoyan Sun, Josef E. Fischer, and Per-Olof Hasselgren

Department of Surgery, University of Cincinnati, and Shriners Hospital for Children, Cincinnati, Ohio 45267

We tested the role of interleukin-6 (IL-6) in sepsis-induced muscle proteolysis by determining ubiquitin mRNA levels and protein breakdown rates in incubated extensor digitorum longus muscles from septic and sham-operated IL-6 knockout and wild-type mice. In addition, the effect of treatment of mice with human recombinant IL-6 on muscle protein breakdown rates was determined. Finally, protein breakdown rates were measured in myotubes treated for up to 48 h with different concentrations of IL-6. Sepsis in wild-type mice resulted in an approximately ninefold increase in plasma IL-6 levels, whereas IL-6 was not detectable in plasma of sham-operated or septic IL-6 knockout mice. Total and myofibrillar muscle protein breakdown rates were increased by ~30% and threefold, respectively, in septic IL-6 wild-type mice with an almost identical response noted in septic IL-6 knockout mice. Ubiquitin mRNA levels determined by dot blot analysis were increased during sepsis in muscles from both IL-6 knockout and wild-type mice, although the increase was less pronounced in IL-6 knockout than in wild-type mice. Treatment of normal mice or of cultured L6 myotubes with IL-6 did not influence protein breakdown rates. The present results suggest that IL-6 does not regulate muscle proteolysis during sepsis.

protein breakdown; ubiquitin; interleukin-6 knockout mice; cytokines; myofibrillar proteins; myotubes


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