Post-traumatic elevation in plasma inflammatory markers, such as high-mobility group protein B1 (HMGB1) and tumor necrosis factor-alpha (TNF-alpha), occurs in parallel with tissue infiltration by activated M1 macrophages and other leukocytes [14, 15], but in burn models of bacterial sepsis, for example, the exaggerated inflammatory response is not always effective at combating infection [16, 17]. This evidence concerns the gene TNF and bacterial infectious disease with sepsis.