Damage- and pathogen-associated molecular patterns and alarmins: keys to sepsis?.
The concept that sepsis is the result of an uncontrolled inflammatory response of the host's innate immune system towards invading pathogens has recently been challenged. Evidence is accumulating that, in addition, host-derived alarm molecules are released during sepsis- and trauma-associated cell death, thus triggering the host's immune response. The identification and characterization of exogenous as well as endogenous danger molecules allowed significant advances in our understanding of the pathophysiology of sepsis and may provide potential targets for therapeutic interventions.
Department of Traumatology, Hand, Plastic and Reconstructive Surgery, University of Ulm, Ulm, Germany.
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Denk
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Perl
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Huber-Lang
D000818:Animals; D001419:Bacteria / Q000472:pathogenicity; D004247:DNA / Q000502:physiology; D005658:Fungi / Q000472:pathogenicity; D024243:HMGB1 Protein / Q000502:physiology; D006657:Histones / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D008928:Mitochondria / Q000502:physiology; D009687:Nuclear Proteins / Q000502:physiology; D000090243:Nucleophosmin; D018805:Sepsis / Q000276:immunology*; D014780:Viruses / Q000472:pathogenicity
D024243:HMGB1 Protein; D006657:Histones; D009687:Nuclear Proteins; D000090243:Nucleophosmin; D004247:DNA