Abstract
Aged mice are less likely to survive following traumatic injury and are more immunosuppressed than young mice who sustain comparable injuries. Immunosuppression in severely injured patients is associated with a TH1–TH2 shift. Young mice had robust delayed-type hypersensitivity (DTH) responses after receiving scald or sham injury, whereas the response was diminished in aged sham-injured mice ( P<0.05), and completely absent in aged burn-injured mice ( P<0.01). Production of interferon-γ (IFN-γ) did not differ between splenocytes from sham-injured young and aged mice. Splenocytes from burn-injured young and aged mice yielded similar (63–68%) decreases in IFN-γ, relative to sham-injured mice ( P<0.05). In the absence of injury, cells from aged mice produced 2-fold more interleukin-4 (IL-4) than cells from young ( P<0.01). Interestingly, after burn, less IL-4 was produced by cell from young and aged mice, when compared to age-matched sham-injured animals ( P<0.05). Further studies revealed that estrogen replacement in aged mice restored the post-injury DTH responses ( P<0.05). Interestingly, this restoration paralleled a recovery in IFN-γ production by splenocytes, but not IL-4 production. Additional studies will be required to determine if age-specific therapies are needed for the treatment of all trauma patients.
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