Temporal analysis of human leucocyte surface antigen expression and neutrophil respiratory burst activity after thermal injury

Sepsis, the major cause of morlidity and mortality after burn injury, is related to multiple immune derangements. Using monoclonal antibodies and two-colour flow cytometry to identify surface antigens, peripheral blood mononuclear cell (PBMC) populations were analysed and correlated with lymphocyte proliferation assays for 21 days postinjury. In addition, in vitro expression of activation antigens by mitogen-stimulated PBMCs was analysed during the time period. Twenty-nine burn patients were studied, with burn injuries ranging from 19 to 97 per cent TBSA; PBMCs from human volunteers were used for control cells. Patients received aggressive enteral nutritional support starting on day 1 postburn and underwent early excision and grafting of wounds; no patients developed sepsis during the study period. The most consistent changes in PBMCs after thermal injury were decreased percentages of total T cells (CD3⁺), T helper/inducer cells (CD4⁺), and T suppressor/cytotoxic cells (CD8⁺); the percentages of natural killer (CD16⁺ ) cells were not altered. Expression of surface 'activation' antigens on CD4⁺ and CD8⁺ cells (HLA-DR, interleukin-2 receptor and transferrin receptor) after mitogen stimulation was significantly depressed as early as 1 day postburn. An early monocytosis was seen on day 1 postburn, but decreases were found on days 4 and 7. Monocyte expression of HLA-DR antigen was suppressed throughout the study. Lymphocyte proliferation after mitogen stimulation and the responses of lymphocytes in mixed lymphocyte culture were suppressed postburn. Neutrophil respiratory burst responses were supranormal on days 1 and 7 postburn, but the differences were not statistically significant. Although burn morbidity and mortality are primarily due to bacterial organisms, defects in T-cell and monocyte immune functions are more predominant than defects in neutrophil bactericidal function in these patients. The block in T-cell blastogenesis is early in the cell cycle, prior to DNA synthesis.