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J Appl Physiol 95: 969-976, 2003. First published May 2, 2003; doi:10.1152/japplphysiol.00005.2003
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M1/70 attenuates blood-borne neutrophil oxidants, activation, and myofiber damage following stretch injury

S. Brickson,1 L. L. Ji,1 K. Schell,2 R. Olabisi,5 B. St. Pierre Schneider,3 and T. M. Best1,4,5,6

1Department of Kinesiology and 3School of Nursing, University of Wisconsin; Departments of 4Orthopedic Surgery, 5Biomedical Engineering, and 6Family Medicine, University of Wisconsin Medical School, Madison 53706; and 2Flow Cytometry Facility, University of Wisconsin Comprehensive Cancer Center, Madison, Wisconsin 53792

Submitted 6 January 2003 ; accepted in final form 30 April 2003

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 after muscle stretch injury by 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 (n = 6), IgG isotype control (n = 3), or saline control (n = 3). After intravenous injection of the assigned agent under gas anesthesia, a standardized single-stretch injury was created in the right tibialis anterior, whereas the left tibialis anterior underwent a sham surgery. Blood-borne neutrophil oxidant generation and CD11b receptor density and plasma IL-8 levels were measured pre- and 24 h postinjury. Damage was assessed histologically at the hematoma site by counting torn myofibers. M1/70 group 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 with IgG isotype or saline control groups. 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 24 h postmuscle stretch injury.

eccentric contraction; chemokine; respiratory burst; CD11b


Address for reprint requests and other correspondence: S. Brickson, Univ. of Wisconsin-Madison, 2000 Observatory Dr., Madison, WI 53706 (E-mail: sbrickson{at}education.wisc.edu).




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