Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:TLR4 signaling is essential for survival in acute lung injury induced by virulent Pseudomonas aeruginosa secreting type III secretory toxins. | Respiratory Research BioMed Central Research Open Access TLR4 signaling is essential for survival in acute lung injury induced by virulent Pseudomonas aeruginosa secreting type III secretory toxins Karine Faure1 Teiji Sawa 2 Temitayo Ajayi3 4 Junichi Fujimoto5 Kiyoshi Moriyama2 Nobuaki Shime6 and Jeanine P Wiener-Kronish2 3 4 Address 1Laboratoire de Recherche en Pathologie Infectieuse Lille France 2Department of Anesthesia and Perioperative Care University of California San Francisco CA 94143 USA 3Department of Medicine University of California San Francisco CA 94143 USA 4Cardiovascular Research Institute University of California San Francisco CA 94143 USA 5Department of Anesthesiology School of Medicine Yokohama City University Yokohama Kanagawa 2360-004 Japan and 6Department of Anesthesiology Kyoto Prefectural University of Medicine Kyoto Kyoto 602-8566 Japan Email Karine Faure - karine-faure@ Teiji Sawa - teiji@ Temitayo Ajayi - tajayi@ Junichi Fujimoto - junfuji@ Kiyoshi Moriyama - kmor7200@ Nobuaki Shime - shime@ Jeanine P Wiener-Kronish - wienerkj@ Corresponding author Published 12 February 2004 Received 02 July 2003 Accepted 12 February 2004 Respiratory Research 2004 5 1 This article is available from http content 5 1 1 2004 Faure et al licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Background The relative contributions of the cytotoxic phenotype of P. aeruginosa expressing type III secretory toxins and an immunocompromised condition lacking normal Toll-like receptor 4 TLR4 signaling in the pathogenesis of acute lung injury and sepsis were evaluated in a mouse model for Pseudomonas aeruginosa pneumonia. By using lipopolysaccharide-resistant C3H
