IMMUNOMECHANISMS OF POSTTRAUMATIC HYPERIN FLAMMATION AND SEPSIS

Major trauma and consecutively associated infectious complications hav e a major impact on the mechanisms of the specific immune response and the nonspecific inflammatory reaction. The trauma-induced host defens e abnormalities become strikingly evident with the analysis of cytokin e synthesis patterns. The dissociation of cell-mediated immune respons es following trauma is based upon an overrepresentation of suppressor- active monocytes and inadequate T-cell help in parallel. Corresponding dysregulation of cytokine production appears within many facets. Comp lement, endotoxin and antigen antibody complexes cause a massive activ ation of monocytes with an abnormal release of essential mediators, li ke PGE2, Il-1, IL-6, IL-8, TGF-beta and TNF-alpha. The regulation of c ytokine synthesis under stressful conditions is differentially regulat ed for the individual mediators, either on a transcriptional or a post transcriptional level. In our opinion, the endogenous provisions of th e organism for survival following major injury are inadequate and from this hypothesis we derive the necessity for a substantial exogenous t herapeutic intervention. The primary target of modern immunotherapy mu st be to inhibit the conversion of a systemic inflammatory reaction in immunocompromised patients towards a status of bacterial sepsis. Diff erent approaches appear to be feasible to avoid the development of lat e multiorgan failure. These interventions have to be utilized preventi vely in a controlled manner as early as possible after trauma has occu rred, and they must effectively protect different cell systems (lympho cytes, monocytes, PMNs and endothelial cells).