Danger Signals Activating the Immune Response after Trauma. (19th June 2012)

• Record Type: Journal Article
• Authors: Hirsiger, Stefanie; Simmen, Hans-Peter; Werner, Clément M. L.; Wanner, Guido A.; Rittirsch, Daniel
• Other Names: Lamkanfi Mohamed Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2012(2012)
• Publication Date: 2012-06-19
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2012/315941
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Sterile injury can cause a systemic inflammatory response syndrome (SIRS) that resembles the host response during sepsis. The inflammatory response following trauma comprises various systems of the human body which are cross-linked with each other within a highly complex network of inflammation. Endogenous danger signals (danger-associated molecular patterns; DAMPs; alarmins) as well as exogenous pathogen-associated molecular patterns (PAMPs) play a crucial role in the initiation of the immune response. With popularization of the "danger theory, " numerous DAMPs and PAMPs and their corresponding pathogen-recognition receptors have been identified. In this paper, we highlight the role of the DAMPs high-mobility group box protein 1 (HMGB1), interleukin-1 α (IL-1 α ), and interleukin-33 (IL-33) as unique dual-function mediators as well as mitochondrial danger signals released upon cellular trauma and necrosis.