Invited review: deterioration of the immune system after trauma: signals and cellular mechanisms.
Multiple trauma leads to a deterioration of the immune system. On the one hand, hyperinflammation mediates remote organ damage and may lead to multi-organ failure. On the other hand, immunosuppression develops and promotes an enhanced risk to acquire infectious complications after trauma. The mechanisms that underlie these opposing consequences of trauma are not yet completely understood. There is increasing evidence that endogenous danger signals that derive from destroyed tissues play a role in trauma-induced immune dysfunction. Here, we give an overview on the common animal models that are used to investigate trauma-induced pathology, potential signals and cellular mechanisms that support the imbalance between inflammation and counter-regulation after trauma.
Flohé
Stefanie B
SB
Surgical Research, Department of Trauma Surgery, University Hospital Essen, University Duisburg-Essen, Essen, Germany. stefanie.flohe@uk-essen.de
Flohé
Sascha
S
Schade
F Ulrich
FU
D000818:Animals; D017951:Antigen Presentation; D003713:Dendritic Cells / Q000276:immunology; D004195:Disease Models, Animal; D024243:HMGB1 Protein / Q000276:immunology; D006360:Heat-Shock Proteins / Q000276:immunology; D006801:Humans; D007107:Immune System / Q000276:immunology* / Q000503:physiopathology; D007111:Immunity, Cellular; D007113:Immunity, Innate; D008264:Macrophages / Q000276:immunology; D009104:Multiple Trauma / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D015398:Signal Transduction / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology
D024243:HMGB1 Protein; D006360:Heat-Shock Proteins