Mortality and sepsis after a traumatic injury is greater in the elderly than in young individuals. The altered lymphocyte response observed to occur in healthy aged individuals is proposed to be a contributing factor to increased mortality. The immune response associated with the increased mortality was explored using a murine scald injury model. In the absence of injury, aged mice had depressed delayed-type hypersensitivity (DTH) and splenocyte proliferative responses relative to young mice. There was also an increase with age in the production of the TH2 cytokines interleukin (IL)-4 and IL-10 by splenocytes. There was no change in the TH1 cytokines IFNgamma or IL-12 with age. However, IL-2 production was significantly lower. Following injury, there was a further decrease in the DTH response of aged injured mice, compared with aged sham mice. In addition, there was a decrease in all of the cytokines examined, regardless of age. In contrast, IFNgamma and IL-2 were significantly lower in the aged injured animals compared with the young injured animals. These results suggest that the lack of an adequate amount of TH1 cytokines shortly after injury in the aged mice may parallel the increased incidence of sepsis and death that occurs in aged burn patients.

These studies suggest that the loss of lymphocyte production of IL-4 after ethanol exposure and burn injury may contribute to the exaggerated production of IL-6, a known mediator of immune suppression after injury. Moreover, the administration of IL-4 may be beneficial for patients with injuries that are characterized by a dysregulated inflammatory response.

These studies suggest that the loss of lymphocyte production of IL-4 after ethanol exposure and burn injury may contribute to the exaggerated production of IL-6, a known mediator of immune suppression after injury. Moreover, the administration of IL-4 may be beneficial for patients with injuries that are characterized by a dysregulated inflammatory response.

No abstract

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