• Johannes Tschöp, André Martignoni, Maria D Reid, Samuel G Adediran, Jason Gardner, Greg J Noel, Cora K Ogle, Alice N Neely, and Charles C Caldwell.
• Department of Research, Shriners Hospital for Children, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0558, USA.
• Shock. 2009 Feb 1; 31 (2): 157163157-63.

AbstractA dysfunctional immune system is known to be part of the pathophysiology after burn trauma. However, reports that support this have used a variety of methods, with numerous variables, to induce thermal injury. We hypothesized that, all other parameters being equal, an injury infliction by a scald would yield different immunological responses than one inflicted by a flame. Here, we demonstrated that both burn methods produced a full-thickness burn, yet there was more of an increase in subdermal temperature, hematocrit, mortality, and serum IL-6 concentrations associated with the scald burn. On postinjury day 1, the scald-burned mice showed diminished lymphocyte numbers, interferon gamma production, and lymphocyte T-bet expression as compared with sham- and flame-burned mice. On postburn day 8, spleens from both sets of thermally injured animals showed an increase in proinflammatory myeloid cells as compared with sham-burned mice. Furthermore, the T-cell numbers, T-bet expression, and phenotype were changed such that interferon gamma production was higher in scald-burned mice than in sham- and flame-burned mice. Altogether, the data show that differential immunological phenotypes were observed depending on the thermal injury method used.

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