title: Severe sepsis and Toll-like receptors.
abstract: Severe sepsis dominates the mortality of non-cardiac intensive care units. The ingenious Toll-like receptor (TLR) system can recognise many infectious organisms through relatively few receptors to trigger pro-inflammatory and anti-inflammatory cytokine release. Further complexity arises from positive and negative signalling feedback loops. Severe sepsis may be a consequence of an inappropriately excessive response or inadequate endogenous negative feedback. Therapies targeting these pathways are currently being evaluated. Alternatively, in clinical scenarios such as compensatory anti-inflammatory response syndrome, chronic viral sepsis or inadequate vaccine function, TLR signalling may be inadequate. TLR agonists may augment the innate response and are being investigated.
authors: Unit of Critical Care Medicine, National Heart and Lung Institute, Imperial College, London, UK.
authors: Hongmei
authors: H
authors: Gao
authors: Susannah K
authors: SK
authors: Leaver
authors: Anne
authors: A
authors: Burke-Gaffney
authors: Simon J
authors: SJ
authors: Finney
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism*; D011110:Polymorphism, Genetic; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism / Q000628:therapy; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology* / Q000378:metabolism
chemical_list: D016207:Cytokines; D051193:Toll-Like Receptors