[Immune mechanisms of post-traumatic hyperinflammation and sepsis]

Major trauma and consecutively associated infectious complications have a major impact on the mechanisms of the specific immune response and the nonspecific inflammatory reaction. The trauma-induced host defense abnormalities become strikingly evident with the analysis of cytokine synthesis patterns. The dissociation of cell-mediated immune responses 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. Complement, endotoxin and antigen antibody complexes cause a massive activation of monocytes with an abnormal release of essential mediators, like PGE2, IL-1, IL-6, IL-8, TGF-beta and TNF-alpha. The regulation of cytokine synthesis under stressful conditions is differentially regulated for the individual mediators, either on a transcriptional or a posttranscriptional level. In our opinion, the endogenous provisions of the organism for survival following major injury are inadequate and from this hypothesis we derive the necessity for a substantial exogenous therapeutic intervention. The primary target of modern immunotherapy must be to inhibit the conversion of a systemic inflammatory reaction in immunocompromised patients towards a status of bacterial sepsis. Different approaches appear to be feasible to avoid the development of late multiorgan failure. These interventions have to be utilized preventively in a controlled manner as early as possible after trauma has occurred, and they must effectively protect different cell systems (lymphocytes, monocytes, PMNs and endothelial cells).