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1 Department of Kinesiology, University of Wisconsin-Madison, Madison, WI, USA
2 Comprehensive Cancer Center, University of Wisconsin-Madison, Madison, WI, USA
3 School of Nursing, University of Wisconsin-Madison, Madison, WI, USA
4 Department of Family Medicine, University of Wisconsin-Madison, Madison, WI, USA; Department of Orthopedic Surgery, University of Wisconsin-Madison, Madison, WI, USA; Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: sbrickson{at}education.wisc.edu.
The purpose of this study was to determine the role of the CD11b-dependent respiratory burst in neutrophil oxidant generation and activation, interleukin-8 (IL-8) production and myofiber damage following muscle stretch injury using the monoclonal antibody M1/70 to block this pathway. Twelve male New Zealand white rabbits were randomly assigned to a treatment group: M1/70 (M, n=6), IgG isotype control (I, n=3) or saline control (S, n=3). Following intravenous injection of the assigned agent under gas anesthesia, a standardized single stretch injury was created in the right tibialis anterior (TA), whereas the left TA underwent a sham surgery. Blood-borne neutrophil oxidant generation and CD11b receptor density, and plasma IL-8 levels were measured pre- and 24h post-injury. Damage was assessed histologically at the hematoma site by counting torn myofibers. M demonstrated decreased blood-borne neutrophil oxidant generation (P<0.05) and CD11b receptor density (P<0.05), an increase in plasma IL-8 concentration (P<0.01), and less torn myofibers (P<0.01) compared to I or S. These data indicate that 1) CD11b-dependent respiratory burst is a major source of oxidants produced by the neutrophil, and that treatment with M1/70 2) attenuates neutrophil activation status, 3) increases plasma IL-8 concentration, and 4) minimizes myofiber damage 24h post-muscle stretch injury.
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