The immunopathogenesis of sepsis

[1]  F. Gruber,et al.  Protective role of phospholipid oxidation products in endotoxin-induced tissue damage , 2002, Nature.

[2]  John D. Fraser,et al.  The Bacterial Superantigen Streptococcal Mitogenic Exotoxin Z Is the Major Immunoactive Agent of Streptococcus pyogenes1 , 2002, The Journal of Immunology.

[3]  D. Annane,et al.  Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. , 2002, JAMA.

[4]  John Land,et al.  Association between mitochondrial dysfunction and severity and outcome of septic shock , 2002, The Lancet.

[5]  S. Akira,et al.  Essential role of MD-2 in LPS responsiveness and TLR4 distribution , 2002, Nature Immunology.

[6]  W. Ruf,et al.  Activation of Endothelial Cell Protease Activated Receptor 1 by the Protein C Pathway , 2002, Science.

[7]  Kathy L. Frees,et al.  Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock. , 2002, Archives of internal medicine.

[8]  M. Vatn,et al.  Association of NOD2 (CARD 15) genotype with clinical course of Crohn's disease: a cohort study , 2002, The Lancet.

[9]  A. Mantovani,et al.  Stimulation of toll-like receptor 4 expression in human mononuclear phagocytes by interferon-gamma: a molecular basis for priming and synergism with bacterial lipopolysaccharide. , 2002, Blood.

[10]  M. Rämet,et al.  Functional genomic analysis of phagocytosis and identification of a Drosophila receptor for E. coli , 2002, Nature.

[11]  M. Belvin,et al.  The Drosophila immune response against Gram-negative bacteria is mediated by a peptidoglycan recognition protein , 2002, Nature.

[12]  P. Detmers,et al.  Toll Receptors: a Central Element in Innate Immune Responses , 2002, Infection and Immunity.

[13]  K. Anderson,et al.  Requirement for a Peptidoglycan Recognition Protein (PGRP) in Relish Activation and Antibacterial Immune Responses in Drosophila , 2002, Science.

[14]  S. Opal,et al.  Bench-to-bedside review: Toll-like receptors and their role in septic shock , 2002, Critical care.

[15]  Y. Ogura,et al.  Nods: a family of cytosolic proteins that regulate the host response to pathogens. , 2002, Current opinion in microbiology.

[16]  Corinne Alberti,et al.  Epidemiology of sepsis and infection in ICU patients from an international multicentre cohort study , 2002, Intensive Care Medicine.

[17]  T. Michel,et al.  Drosophila Toll is activated by Gram-positive bacteria through a circulating peptidoglycan recognition protein , 2001, Nature.

[18]  K. Okajima Regulation of inflammatory responses by natural anticoagulants , 2001, Immunological reviews.

[19]  M Schetz,et al.  Intensive insulin therapy in critically ill patients. , 2001, The New England journal of medicine.

[20]  E. Ivers,et al.  Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock , 2001 .

[21]  A. Norrby-Teglund,et al.  Evidence for superantigen involvement in severe group a streptococcal tissue infections. , 2001, The Journal of infectious diseases.

[22]  D. Landry,et al.  The pathogenesis of vasodilatory shock. , 2001, The New England journal of medicine.

[23]  C. Esmon,et al.  Dysfunction of endothelial protein C activation in severe meningococcal sepsis. , 2001, The New England journal of medicine.

[24]  S. Akira,et al.  Human TLR9 confers responsiveness to bacterial DNA via species-specific CpG motif recognition , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[25]  G. Clermont,et al.  Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care , 2001, Critical care medicine.

[26]  J. Cavaillon,et al.  Pyrogenicity and Cytokine-Inducing Properties ofStreptococcus pyogenes Superantigens: Comparative Study of Streptococcal Mitogenic Exotoxin Z and Pyrogenic Exotoxin A , 2001, Infection and Immunity.

[27]  R. Hotchkiss,et al.  Sepsis-Induced Apoptosis Causes Progressive Profound Depletion of B and CD4+ T Lymphocytes in Humans1 , 2001, The Journal of Immunology.

[28]  M. Colonna,et al.  TREM-1 amplifies inflammation and is a crucial mediator of septic shock , 2001, Nature.

[29]  S. Akira,et al.  The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5 , 2001, Nature.

[30]  K. Tracey,et al.  HMG‐1 REDISCOVERED AS A CYTOKINE , 2001, Shock.

[31]  J Ean,et al.  Efficacy and safety of recombinant human activated protein C for severe sepsis. , 2001, The New England journal of medicine.

[32]  M. Dinges,et al.  Role of T Cells and Gamma Interferon during Induction of Hypersensitivity to Lipopolysaccharide by Toxic Shock Syndrome Toxin 1 in Mice , 2001, Infection and Immunity.

[33]  T. Hartung,et al.  Structure-function relationship of cytokine induction by lipoteichoic acid from Staphylococcus aureus. , 2001 .

[34]  F. Stüber Effects of genomic polymorphisms on the course of sepsis: is there a concept for gene therapy? , 2001, Journal of the American Society of Nephrology : JASN.

[35]  Y. Ogura,et al.  Human Nod1 Confers Responsiveness to Bacterial Lipopolysaccharides* , 2001, The Journal of Biological Chemistry.

[36]  K. Murthy,et al.  Flagellin, a Novel Mediator of Salmonella-Induced Epithelial Activation and Systemic Inflammation: IκBα Degradation, Induction of Nitric Oxide Synthase, Induction of Proinflammatory Mediators, and Cardiovascular Dysfunction1 , 2001, The Journal of Immunology.

[37]  A. Aderem,et al.  The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between toll-like receptors. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[38]  D. Hultmark,et al.  A family of peptidoglycan recognition proteins in the fruit fly Drosophila melanogaster. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[39]  J. Mira,et al.  A Novel Polymorphism in the Toll-Like Receptor 2 Gene and Its Potential Association with Staphylococcal Infection , 2000, Infection and Immunity.

[40]  A. Aderem,et al.  Toll-like receptors in the induction of the innate immune response , 2000, Nature.

[41]  K. Acharya,et al.  Microbial superantigens: from structure to function. , 2000, Trends in microbiology.

[42]  S. Foster,et al.  Peptidoglycan and Lipoteichoic Acid from Staphylococcus aureus Induce Tumor Necrosis Factor Alpha, Interleukin 6 (IL-6), and IL-10 Production in Both T Cells and Monocytes in a Human Whole Blood Model , 2000, Infection and Immunity.

[43]  M. Colonna,et al.  Cutting Edge: Inflammatory Responses Can Be Triggered by TREM-1, a Novel Receptor Expressed on Neutrophils and Monocytes1 , 2000, The Journal of Immunology.

[44]  K. Fukase,et al.  Intrinsic conformation of lipid A is responsible for agonistic and antagonistic activity. , 2000, European journal of biochemistry.

[45]  A. Bowie,et al.  The interleukin‐1 receptor/Toll‐like receptor superfamily: signal generators for pro‐inflammatory interleukins and microbial products , 2000, Journal of leukocyte biology.

[46]  R. Bucala,et al.  Protection from septic shock by neutralization of macrophage migration inhibitory factor , 2000, Nature Medicine.

[47]  S. Korsmeyer,et al.  Prevention of lymphocyte cell death in sepsis improves survival in mice. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[48]  T. van der Poll,et al.  Pathogenesis of DIC in Sepsis , 1999 .

[49]  S. Akira,et al.  Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components. , 1999, Immunity.

[50]  T. van der Poll,et al.  Disseminated Intravascular Coagulation , 1999, Thrombosis and Haemostasis.

[51]  K. Tracey,et al.  HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.

[52]  R. Hotchkiss,et al.  Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. , 1999, Critical care medicine.

[53]  Yoshinori Nagai,et al.  MD-2, a Molecule that Confers Lipopolysaccharide Responsiveness on Toll-like Receptor 4 , 1999, The Journal of experimental medicine.

[54]  H. Langen,et al.  Digestion of Streptococcus pneumoniae Cell Walls with Its Major Peptidoglycan Hydrolase Releases Branched Stem Peptides Carrying Proinflammatory Activity* , 1999, The Journal of Biological Chemistry.

[55]  R. Sékaly,et al.  Understanding the mechanism of action of bacterial superantigens from a decade of research , 1999, Immunological reviews.

[56]  A. Satoskar,et al.  Targeted Disruption of Migration Inhibitory Factor Gene Reveals Its Critical Role in Sepsis , 1999, The Journal of experimental medicine.

[57]  P. Ricciardi-Castagnoli,et al.  Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. , 1998, Science.

[58]  C. Janeway,et al.  Introduction: the role of innate immunity in the adaptive immune response , 1998, Seminars in immunology.

[59]  R. Bucala,et al.  Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of Gram-positive bacteria. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[60]  A. Devitt,et al.  Human CD14 mediates recognition and phagocytosis of apoptotic cells , 1998, Nature.

[61]  L. Björck,et al.  Activation of the contact-phase system on bacterial surfaces—a clue to serious complications in infectious diseases , 1998, Nature Medicine.

[62]  C. Dinarello,et al.  Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. , 1997, Chest.

[63]  C. Janeway,et al.  A human homologue of the Drosophila Toll protein signals activation of adaptive immunity , 1997, Nature.

[64]  K. Asadullah,et al.  Monocyte deactivation in septic patients: Restoration by IFN-γ treatment , 1997, Nature Medicine.

[65]  K. Heeg,et al.  Bacterial DNA causes septic shock , 1997, Nature.

[66]  E. Hailman,et al.  Lipopolysaccharide binding protein and soluble CD14 catalyze exchange of phospholipids. , 1997, The Journal of clinical investigation.

[67]  R. Ulevitch,et al.  Antibodies against CD14 protect primates from endotoxin-induced shock. , 1996, The Journal of clinical investigation.

[68]  J. Bernhagen,et al.  MIF as a glucocorticoid-induced modulator of cytokine production , 1995, Nature.

[69]  R. Landmann,et al.  Increased circulating soluble CD14 is associated with high mortality in gram-negative septic shock. , 1995, The Journal of infectious diseases.

[70]  A. Tomasz,et al.  CD14 is a pattern recognition receptor. , 1994, Immunity.

[71]  R. Ulevitch,et al.  CD14, a receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein. , 1990, Science.

[72]  B. Bistrian,et al.  Intensive insulin therapy in critically ill patients. , 2002, The New England journal of medicine.

[73]  R. Dziarski,et al.  Peptidoglycan Recognition Proteins A NOVEL FAMILY OF FOUR HUMAN INNATE IMMUNITY PATTERN RECOGNITION MOLECULES* , 2001 .

[74]  J. Cohen,et al.  Adjunctive therapy in sepsis: a critical analysis of the clinical trial programme. , 1999, British medical bulletin.

[75]  M. Kotb,et al.  Bacterial pyrogenic exotoxins as superantigens , 1995, Clinical microbiology reviews.