Sepsis: avoiding its deadly toll.
Systemic bacterial infection may culminate in a frequently fatal septic shock syndrome. The underlying pathology is the result of an uncontrolled inflammatory response, stimulated by the pathogen and its products. Toll-like receptors (TLRs) are critically involved in sensing bacteria and, in the case of sepsis, stimulate a pathogenic response by the innate immune system. A new study reports a successful attempt to inhibit systemic inflammation in mice by disrupting the formation of complexes between Gram-positive bacteria and their cognate receptor, TLR2.
Decker
Thomas
T
Max F. Perutz Laboratories, University Departments at the Vienna Biocenter, Department of Microbiology and Genetics, University of Vienna, Vienna, Austria. thomas.decker@univie.ac.at
D000818:Animals; D006094:Gram-Positive Bacteria / Q000472:pathogenicity; D006801:Humans; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D011956:Receptors, Cell Surface / Q000037:antagonists & inhibitors / Q000502:physiology; D018805:Sepsis / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D012772:Shock, Septic / Q000209:etiology / Q000276:immunology; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors
D018836:Inflammation Mediators; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors