title: The impact of endogenous triggers on trauma-associated inflammation.
abstract: OBJECTIVE
  Inflammation immediately starting after trauma is a consequence of an efficient host defense system that is not only capable of sensing exogenous and pathogen-derived danger signals, but also endogenous, multifunctional alarm signals, which both can initiate an inflammatory response.
  
  
  RESULTS
  Even in the absence of infection, Toll-like receptors play an important role in inflammation via recognition of host-derived, endogenous 'damage signals' like heat shock proteins and 'alarmins' such as the nuclear protein high-mobility group box protein 1, which are presented as a result of tissue trauma. In addition to the Toll-like receptors, a number of other receptors are involved in the host inflammatory response, including the new family of nucleotide oligomerization domain-like receptors capable of sensing the presence of danger signals in the cytoplasm. Important links occur between the Toll-like receptors as key inducers of the pro-forms of interleukin-1beta and interleukin-18 and the activation of certain nucleotide oligomerization domain-like receptors, resulting in inflammasome formation--an essential process leading to the secretion of these proinflammatory cytokines.
  
  
  CONCLUSIONS
  In addition to improved insights into the regulation of traumatic inflammation and the etiology of the systemic inflammatory response syndrome, some endogenous immune triggers seem to have the potential to serve as novel biomarkers in predicting post-traumatic complications.
authors.affiliation: Klinikum Grosshadern, Ludwig-Maximilians-University of Munich, Department of Surgery, Munich, Germany.
authors.forename: Siegfried
authors.initials: S
authors.lastname: Zedler
authors.forename: Eugen
authors.initials: E
authors.lastname: Faist
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000276:immunology / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D051017:Apoptosis Regulatory Proteins / Q000276:immunology / Q000502:physiology; D015415:Biomarkers; D016207:Cytokines / Q000276:immunology / Q000502:physiology*; D024243:HMGB1 Protein / Q000276:immunology / Q000502:physiology; D006360:Heat-Shock Proteins / Q000276:immunology / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D007378:Interleukins / Q000276:immunology / Q000502:physiology; D000070576:NLR Proteins; D053472:Nod Signaling Adaptor Proteins / Q000276:immunology / Q000502:physiology; D051193:Toll-Like Receptors / Q000276:immunology / Q000502:physiology; D014947:Wounds and Injuries / Q000276:immunology / Q000503:physiopathology*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D051017:Apoptosis Regulatory Proteins; D015415:Biomarkers; D016207:Cytokines; D024243:HMGB1 Protein; D006360:Heat-Shock Proteins; D007378:Interleukins; D000070576:NLR Proteins; C427903:NLRP1 protein, human; D053472:Nod Signaling Adaptor Proteins; D051193:Toll-Like Receptors