Depressed cell-mediated and humoral immune functions have been reported to occur following severe thermal and traumatic injury. In this study we have questioned whether another immune function, natural killing (NK), is also disturbed in these injured patients. Twenty-two thermally injured patients with burns ranging from 5 to 75% of the total body surface area and 15 traumatically injured patients with injury severity scores ranging from 9 to 56 were followed postinjury and compared to 29 age-matched controls. NK activity was measured as the percentage cytotoxicity in chromium-51 release assays with K562 target cells. The more severely burned patients had significantly depressed NK activity for the 40-day period following injury that remained reduced for the duration of the study. Patients with lesser burns had reduced NK-cell function for the initial 10-day period postburn that returned slowly to the normal range. Traumatically injured patients had depressed NK-cell function during the 3- to 6-day period postinjury. The percentage of cells bearing phenotypic markers for the groups in which NK cells are found was either normal or elevated in these patients. A correlation was found between NK activity and interleukin 2 generation by mononuclear cells from these patients. In order to investigate the mechanism of NK suppression in these patients, NK-cell function was studied following the infusion of cortisol, epinephrine, and glucagon into volunteer subjects in amounts known to reproduce serum levels seen following injury of moderate severity. NK-cell function was reduced an average of 66% following infusion, suggesting that the inhibition of NK-cell function seen in patients may be mediated by the stress response to injury.
Depression of cell-mediated immunity in patients following severe traumatic injury has been well documented in vitro and in vivo. However, the exact mechanism of this defect is still controversial. In this study, we have investigated the ability of injured patients' peripheral blood mononuclear cells (PBMC) to produce two important immunoregulatory molecules, interleukin 1 (IL 1) and interleukin 2 (IL 2). Eighteen traumatic injury patients were studied during the course of their hospital stay and their results compared with a group of 18 normal age- and sex-matched controls. The results showed the following. (1) Production of IL 2 by normal PBMC in response to optimal doses of mitogen may vary with sex as well as age. (2) Adherent mononuclear cells from trauma patients produced at least as much IL 1 as normals. (3) IL 2 production, however, was markedly suppressed (normals, 1.6 +/- 0.2 U; traumatic injury, 0.6 +/- 0.1 U; P = 0.001) and persisted for as long as 50 days postinjury. OKT4+ cells were not significantly decreased at any time, nor were OKT8+ suppressor/cytotoxic cells increased at any time. Decreased IL 2 production in patients treated with steroids or those who were septic was not different from that in those patients who were not treated with steroids or were not septic. These results suggest that the cause of the defect in IL 2 production in traumatic injury patients is not related to a lack of the IL 1 signal, producer T cells, or Ia+ monocytes or to increased suppressor T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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