The purpose of this study was to determine the role of the CD11b-dependent respiratory burst in neutrophil oxidant generation and activation, @entity20574 ( @entity20574 ) production, and @entity16 after @entity121 by using the monoclonal antibody M1/70 to block this pathway. Twelve male New Zealand White @entity95 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- @entity130 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 @entity20574 levels were measured pre- and 24 h postinjury. Damage was assessed histologically at the @entity1410 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 @entity20574 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 @entity20574 concentration, and 4). minimizes @entity16 24 h postmuscle @entity130 .

M1/70 attenuates blood-borne neutrophil oxidants, activation, and XXXX following @entity130 .

@entity16 :: ('MESH:D009422', 'Disease') :: ['myofiber damage'] @entity95 :: ('9986', 'Species') :: ['rabbits'] @entity1410 :: ('MESH:D006406', 'Disease') :: ['hematoma'] @entity20574 :: ('100009129(Tax:9986)', 'Gene') :: ['IL-8', 'interleukin-8'] @entity121 :: ('MESH:D009135', 'Disease') :: ['muscle stretch injury'] @entity130 :: ('MESH:D014947', 'Disease') :: ['stretch injury']
@entity16 :: (MESH:D009422,Disease) :: ['myofiber damage']
