Does burn wound excision after thermal injury attenuate subsequent macrophage hyperactivity and immunosuppression?
Studies have shown that cell mediated immunity is suppressed markedly following thermal injury. Macrophages and the activation of an inflammatory cascade that includes interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNFalpha) and PGE2 have been implicated as causative factors. Burn wound excision and grafting is a common clinical practice that decreases patient morbidity and mortality. It is not known, however, if the salutary effects of this procedure are related to modulation of macrophage activity post-burn. Therefore, C57BL/6 female mice were subjected to a third-degree scald burn covering 25% of their total body surface area followed by complete excision 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 TNFalpha, IL-6, nitric oxide, and PGE2 production in response to lipopolysaccharide stimulation, whereas IL-1beta production was not increased. Burn wound excision and grafting normalized TNFalpha production to sham levels, independent of when post-burn the procedure was conducted. In contrast, the elevated production of other inflammatory mediators (IL-1beta, IL-6, nitric oxide, PGE2) post-burn was unaffected by burn wound excision and grafting. Moreover, splenic T-lymphocyte proliferation was also suppressed at 7 days post-burn and was not improved by burn wound excision and grafting. These results, therefore, suggest that the beneficial effects of burn wound excision and grafting are likely to be related to the normalization of macrophage TNFalpha production as well as the maintenance of skin barrier function.
Schwacha
M G
MG
Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, 35294-0019, USA.
Knöferl
M W
MW
Chaudry
I H
IH
D000818:Animals; D002056:Burns / Q000276:immunology* / Q000601:surgery*; D015232:Dinoprostone / Q000096:biosynthesis; D005260:Female; D006358:Hot Temperature; D007108:Immune Tolerance; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity; D008213:Lymphocyte Activation / Q000187:drug effects; D008262:Macrophage Activation / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000096:biosynthesis; D016038:Skin Transplantation; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D014185:Transplantation, Isogeneic; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D015232:Dinoprostone