The role of the neutrophil following single stretch injury.

摘要

Single stretch muscle injuries occur frequently and with a high morbidity rate, yet little is known about the underlying pathophysiology. It has been suggested that oxidants produced by neutrophils may play a role either by acting directly to damage myofibers or as signaling intermediates to augment the inflammatory response.; The first study identified the time course for specific types of inflammatory cells following single stretch injury. Neutrophils were reported to be the predominant cell type to infiltrate injured myofibers 24h post-injury. The role of neutrophil-derived oxidants on myofiber damage and as signaling intermediates was then evaluated using the anti-CD11b monoclonal antibody M1/70 to block the respiratory burst. The presence of neutrophils in injured muscle was attenuated in M1/70-treated animals and associated with less myofiber damage, as assessed by torn fibers, and loss of the cytoskeletal proteins desmin and dystrophin. Oxidants were also shown to be a critical signal for inflammation. M1/70 treated-animals demonstrated less neutrophil activation, as assessed by CD11b receptor density, and interleukin 8 tissue levels.; In summary, this work demonstrated a causal link between neutrophils and myofiber damage, although oxidants could not be confirmed as the sole contributing factor. Oxidants were shown to play a critical feed-forward role in determining neutrophil activation and tissue levels of interleukin 8, which may ultimately increase the capacitance of the neutrophil to elicit damage.