Does burn wound excision after thermal injury attenuate subsequent macrophage hyperactivity and immunosuppression?

Studies have shown that cell mediated immunity is suppressed markedly follo wing thermal injury. Macrophages and the activation of an inflammatory casc ade that includes interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TN F alpha) and PGE(2) have been implicated as causative factors. Burn wound e xcision and grafting is a common clinical practice that decreases patient m orbidity and mortality. It is not known, however, if the salutary effects o f this procedure are related to modulation of macrophage activity post-burn . Therefore, C57BL/6 female mice were subjected to a third-degree scald bur n covering 25% of their total body surface area followed by complete excisi on and allografting of the injury site at 8, 24, or 72 h post-burn. Splenic macrophage function was assessed 7 days post-burn. Thermal injury without burn excision and grafting significantly increased macrophage TNF alpha, IL -6, nitric oxide, and PGE(2) production in response to lipopolysaccharide s timulation, whereas IL-1 beta production was not increased. Burn wound exci sion and grafting normalized TNF alpha production to sham levels, independe nt of when post-burn the procedure was conducted. In contrast, the elevated production of other inflammatory mediators (IL-1 beta, IL-6, nitric oxide, PGE(2)) post-burn was unaffected by burn wound excision and grafting. More over, splenic T-lymphocyte proliferation was also suppressed at 7 days post -burn and was not improved by burn wound excision and grafting. These resul ts, therefore, suggest that the beneficial effects of burn wound excision a nd grafting are likely to be related to the normalization of macrophage TNF alpha production as well as the maintenance of skin barrier function.