We measured plasma levels of interieukin-1l6 (IL-1j5), tumor necrosis factor a (TNFa), and interdeukin-6 (IL-6) following thermal injury. Cytokine levels In the plasma of 27 burned patients were serially screened by ELISA and compared with cytokine levels > in 16 healthy laboratory employees. The relationships between cytokine_ (.0 concentrations and patient mortality, bum size, and time postbum were examined. Plasma samples with detectable amounts of IL-1ft and IL-6 were significantly more frequent in burned patients than In controls, whereas TNFa was undetectable in most plasma samples. All nonsurviving burned patients had detectable -6 levels; theseSt were significantly higher than those of surviving patients. The IL-1# and IL-6 concentrations were highest during the first week after injury and declined over time. The IL-18 concentrations were positively correlated with bum size. These findings ___ suggest that IL-16 and IL-6 may influence metabolic and Immunologic responses in the first few weeks following thermal Injury. Tumor necrosis factor a was transiently Q elevated in a small subpopulation of burned patients with no obvious relationship to MM bum size or time posthum.r
Injury elicits a response from all cells of the immune system in which cytokines and other metabolic products of activated leukocytes can act either beneficially to provide for enhanced host resistance or deleteriously to depress the function of remote organs and cause what has been termed systemic inflammation. These at times antithecal responses of leukocytes that appear to integrate postinjury changes in the neuroendocrine, immune, and coagulation systems have been implicated as principal causative factors in multiple systems organ failure. Numerous investigators have evaluated a variety of therapeutic agents to prevent and control infection by restoring leukocyte function, while others have evaluated antagonists and monoclonal antibodies as a means of controlling the exaggerated and persistent actions of leukocytes and cytokines caused by systemic inflammation. The redundancies of the cell populations and tie cytokines and other metabolites produced by the cells predictably limit the effectiveness of any single agent and make clinical evaluation of such agents difficult.
We studied the effects of granulocyte-macrophage colonygranulocyte dysfunction may contribute significantly to the stimulating factor In burn patients. Serial measurements of granmarked predisposition to infection. ' ulocyte oxidative function were obtained In treated patients and Granulocyte-macrophage colony-stimulating factor (GMin a group of controls matched for age and total bum size. The CSF) is a lymphokine that was first described nearly 20 years administration of 4granulocyte-macrophage colony-stimulating
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