Severe sepsis and Toll-like receptors.
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.
Gao
Hongmei
H
Unit of Critical Care Medicine, National Heart and Lung Institute, Imperial College, London, UK.
Leaver
Susannah K
SK
Burke-Gaffney
Anne
A
Finney
Simon J
SJ
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
D016207:Cytokines; D051193:Toll-Like Receptors