The immunological effects of trauma

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Trauma, both surgical as occurs during an elective operation, and accidental as in the burn or road traffic accident victim, is associated with a relative state of immunosuppression. Why this apparently deleterious response should happen remains unexplained, but our understanding of the interactions within the immune system during trauma is increasing dramatically. The use of monoclonal antibodies, recombinant DNA technology and highly sensitive assays has permitted the dissection of much of the immune system to be carried out. The present review will examine recent findings on the immunological consequences of trauma. For many years surgeons have been aware that patients who have short, uncomplicated operations recover much quicker than those who have lengthy, complex procedures (Buckman, 1976). The metabolic (Gill et al. 1975) and endocrine (Johnston, 1972) responses to trauma are well known. Recent interest in the immune system (which has an important role in response to infection, allograft rejection and probably malignancy) and trauma has developed because of the exciting possibility of using drugs or cytokines to block or augment certain immunological events. The immunological response can be seen as an orderly progression of cellular activity and protein production to control injury and modulate healing. This includes haemostasis, production of growth factors, changes in the microcirculation, the inflammatory response and wound repair. The inflammatory response can be subdivided into an innate response and an adaptive one. The innate response includes such factors as secreted enzymes and proteins, acute-phase proteins, activation of the alternate pathways of complement, the interferons (IFN) and non-specific immunological activity such as phagocytosis and natural killer (NK) cell activity. None of the factors previously described require previous ‘programming’ or cooperation with specific antigen-primed cells to be effective. The adaptive immune response, in contrast, is a highly specific response occurring as a result of directed antibodies, targeted cytokine-mediated lymphocyte activity and the classical pathway of complement activation (Lennard, 1991). The typical cascade reaction to antigen is shown in Fig. 1.