Translocation of bacterial NOD2 agonist and its link with inflammation 英文参考文献.docVIP

Available online /content/13/4/R124 Research Open Access Vol 13 No 4 Translocation of bacterial NOD2 agonist and its link with inflammation Oh Yoen Kim1, Antoine Monsel2, Michèle Bertrand2, Jean-Marc Cavaillon1, Pierre Coriat2 and Minou Adib-Conquy1 1Cytokines Inflammation Unit, Institut Pasteur, 28 rue Dr. Roux, 75015 Paris, France 2Department of Anesthesiology and Critical Care, Université Pierre et Marie Curie – Paris 6, and Centre Hospitalier Universitaire Pitié-Salpêtrière, Assistance-Publique H?pitaux de Paris, Paris, France Corresponding author: Jean-Marc Cavaillon, jmcavail@pasteur.fr Received: 28 May 2009 Revisions requested: 3 Jul 2009 Revisions received: 9 Jul 2009 Accepted: 28 Jul 2009 Published: 28 Jul 2009 Critical Care 2009, 13:R124 (doi:10.1186/cc7980) This article is online at: /content/13/4/R124 ? 2009 Kim et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction The gut is often considered as the motor of critical illness through bacterial translocation, which amplifies the inflammatory response and alters the immune status. However, Results In 90.5% of the AAS patients, a NOD2 agonist peak was detected in plasma before aortic clamping, but after gut manipulation by the surgeon, and persisted after blood reperfusion. As expected, no peak was detected in plasma from CAS patients (P = 0.003). Leukocyte-bound endotoxin systemic bacterial translocation was rarely proven and endotoxin measurement only reflects translocation of Gram- negative-derived frequently identified if peptidoglycan, derived from both Gram- negative and Gram-positive bacteria, was measured. products. The process could be more appeared after blood reperfusion in 7