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M1/70 attenuates blood-borne neutrophil oxidants, activation, and myofiber damage following stretch injury

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

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