Injury elicits a response from all cells of the immune system in which
cytokines and other metabolic products of activated leukocytes can ac
t either beneficially to provide for enhanced host resistance or delet
eriously to depress the function of remote organs and cause what has b
een termed systemic inflammation. These at times antithecal responses
of leukocytes that appear to integrate postinjury changes in the neuro
endocrine, immune, and coagulation systems have been implicated as pri
ncipal causative factors in multiple systems organ failure. Numerous i
nvestigators have evaluated a variety of therapeutic agents to prevent
and control infection by restoring leukocyte function, while others h
ave evaluated antagonists and monoclonal antibodies as a means of cont
rolling the exaggerated and persistent actions of leukocytes and cytok
ines caused by systemic inflammation. The redundancies of the cell pop
ulations and the cytokines and other metabolites produced by the cells
predictably limit the effectiveness of any single agent and make clin
ical evaluation of such agents difficult.