Depressed Immune Response in Burn Patients

Abstract

Recent experimental evidence has suggested that circulating suppressor leukocytes play an important role in mediating the suppression of immunity seen in burn patients. In order to shed further light on the relationship between suppressor cells and depressed cellular immunity 22 patients were studied (mean age 37) who had suffered severe burns of greater than 30% body surface area. Simultaneous studies were performed on 14 control laboratory personnel (mean age 32). Monoclonal antibodies were used to identify T-lymphocyte subsets known to have suppressor/cytotoxic (OKT8) and helper/inducer (OKT4) function, respectively. In addition, serial measurements were made of the response of circulating lymphocytes to the T-cell mitogen phytohemagglutinin (PHA). An inversion of the normal ratio between suppressor/cytotoxic and helper/inducer subsets (normal 0.55:1, postburn 1.4:1; p less than 0.001) occurred soon after burn injury, reached a peak in five to seven days and then returned gradually to normal levels by 14 days. A diminished response of patients' lymphocytes to PHA (57 +/- 10% SD suppression as compared with normal controls at five to seven days) corresponded with high suppressor to helper cell ratios and returned to normal at the same time. Functional assays, which recognize only high levels of activity, demonstrated circulating suppressor cells in nine patients during this same period but became negative by 14 days. These early immunologic modulations were not predictive of morbidity or mortality. Later in the postburn course, systemic sepsis in eight patients was associated with a return of increased suppressor to helper cell ratios and decreased mitogen (PHA) responsiveness. At this time functional assays demonstrated circulating suppressor cells in six patients. Five of these six patients died of sepsis. It was concluded that severe burn injury regularly induces an early transient increase in circulating suppressor cells accompanied by a depression of lymphocyte activation. A later (greater than 14 days postburn) increase in suppressor cells to levels detectable by functional assays is closely correlated with mortality from sepsis.

Effect of Probiotic Supplementation on Bacterial Translocation in Thermal Injury

“…Lysosomal enzymes and free oxygen radicals are released after hypoxia, leading to the development of intestinal mucosal lesions, a decrease in mucus secretion, deterioration of intestinal barrier function, and finally BT. [23][24][25] Accordingly, our group 2 had significantly greater BT and significantly worse mucosal damage than the other groups. Sepsis and septic complications increase mortality and morbidity after thermal injury.…”

“…Sepsis and septic complications increase mortality and morbidity after thermal injury. 2,10,11,24,26 Recent studies on immunoprotective enteral diets have shown that they provide both metabolic and immunological support for such patients. [9][10][11]27 Choudhry et al suggested that a diet enriched with immunocompounds, such as arginine, fish oil, nucleotides, and glutamine can prevent T-cell dysfunction after thermal injury.…”

Serial Mixed Lymphocyte Culture Responses in Pigs after Liver or Kidney Auto- or Allotransplantation

“…The universal control pair was retained through out the experiment so that in sequential tests lympho cytes from experimental pigs were always mixed with the same universal control pair. Mixed lymphocyte cultures were prepared as follows: the technique for three-way MLC was based on the methods of Miller and Baker [14], Mclrvine et al [15], and Thurman et al [ 16]. Fresh lymphocytes were always used as cryopreserved pig lymphocytes do not function as well as fresh cells in the MLC [17].…”