Stress molecules in sepsis and systemic inflammatory response syndrome
- 4 April 2007
- journal article
- review article
- Published by Wiley in FEBS Letters
- Vol. 581 (19) , 3723-3733
- https://doi.org/10.1016/j.febslet.2007.03.074
Abstract
During sepsis, microbial derived products ("pathogen-associated molecular patterns", PAMPs) are recognized as exogenous danger signals by specific sensors of the host ("pattern recognitions receptors", PRRs). This interaction leads to the release of numerous stress proteins that are a prerequisite to fight infection, though their overzealous production can contribute to tissue damage, organ dysfunction and eventually death. In critically ill patients, translocation of PAMPs can occur from the gut, and injured tissues and cells release endogenous danger signals called "alarmins" (e.g. High mobility group box-1); that share some properties with PAMPs. Thus, numerous similarities occur during infectious and non-infectious systemic inflammation.Keywords
This publication has 65 references indexed in Scilit:
- Role of HMGB1 in apoptosis-mediated sepsis lethalityThe Journal of Experimental Medicine, 2006
- Soluble MD-2 activity in plasma from patients with severe sepsis and septic shockBlood, 2004
- LPS-binding protein-deficient mice have an impaired defense against Gram-negative but not Gram-positive pneumoniaInternational Immunology, 2004
- Disturbed Homeostasis of Lung Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1 During SepsisPublished by Elsevier ,2004
- Overexpression of Interleukin‐15 Protects againstEscherichia coli–Induced Shock Accompanied by Inhibition of Tumor Necrosis Factor–α–Induced ApoptosisThe Journal of Infectious Diseases, 2003
- Nicotinic acetylcholine receptor α7 subunit is an essential regulator of inflammationNature, 2002
- Administration of two macrophage-derived interferon-γ-inducing factors (IL-12 and IL-15) induces a lethal systemic inflammatory response in mice that is dependent on natural killer cells but does not require interferon-γCellular Immunology, 2002
- Elevated Plasma Concentrations of Interferon (IFN)–γ and the IFN‐γ–Inducing Cytokines Interleukin (IL)–18, IL‐12, and IL‐15 in Severe MelioidosisThe Journal of Infectious Diseases, 1999
- LOW HLA-DR EXPRESSION ON MONOCYTES AS A PROGNOSTIC MARKER FOR BACTERIAL SEPSIS AFTER LIVER TRANSPLANTATIONTransplantation, 1997
- Triggering through CD40 promotes interleukin-4-induced CD23 production and enhanced soluble CD23 release in atopic diseaseEuropean Journal of Immunology, 1996