Mechanisms of immune failure in burn injury

The burden on military medical services in handling burn casualties is daunting as all physiological systems become affected. Severe burns in a battlefield setting have a very low salvage rate, to a great degree because of the immune failure which invariably develops. Evaluations of responses of lymphocytes taken from burn patients over several weeks following the burn (> 30% total burn surface area), have revealed that the immune failure which follows thermal injury involves T-cell activation events. Interleukin 2, which is normally produced by activated T lymphocytes, is very poorly produced by cells cultivated in vitro taken from non-surviving patients, whereas some production continues, although at below normal levels, in patients who ultimately survive their injury. IL2 exogenously added to lymphocyte cultures enhances the proliferation of cells from surviving patients but gives no such help to cells from non-survivors. The TAC portion of the IL2 receptor (IL2R alpha), expressed on the T-cell surface, appears to be responsible for this difference, as the number of lymphocytes able to express IL2R alpha falls post-burn. A lipid protein complex (LPC) produced in skin by burning has been shown to inhibit the immune response in vivo and the growth of IL2-dependent lymphocytes in culture. Cerium nitrate, applied topically to the burn patient, is thought to fix the LPC in the burn eschar and prevent its entry into the circulation. In a study of ten patients, bathed in cerium nitrate, some T-lymphocyte activities were found to be in the normal range rather than suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)