[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).
Faist
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Chirurgische Klinik und Poliklinik, Klinikum Grosshadern, Universität München.
Hartl
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WH
Baue
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AE
D003115:Colony-Stimulating Factors / Q000627:therapeutic use; D005936:Glucans / Q000627:therapeutic use; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use; D007167:Immunotherapy; D007371:Interferon-gamma / Q000627:therapeutic use; D007978:Levamisole / Q000627:therapeutic use; D010431:Pentoxifylline / Q000627:therapeutic use; D014947:Wounds and Injuries / Q000276:immunology* / Q000382:microbiology* / Q000628:therapy
D003115:Colony-Stimulating Factors; D005936:Glucans; D007155:Immunologic Factors; D007978:Levamisole; D007371:Interferon-gamma; D010431:Pentoxifylline
Immunmechanistik der posttraumatischen Hyperinflammation und Sepsis.