Harmful molecular mechanisms in sepsis.
Sepsis and sepsis-associated multi-organ failure are major challenges for scientists and clinicians and are a tremendous burden for health-care systems. Despite extensive basic research and clinical studies, the pathophysiology of sepsis is still poorly understood. We are now beginning to understand that sepsis is a heterogeneous, dynamic syndrome caused by imbalances in the 'inflammatory network'. In this Review, we highlight recent insights into the molecular interactions that occur during sepsis and attempt to unravel the nature of the dysregulated immune response during sepsis.
Rittirsch
Daniel
D
Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, Michigan 48109-0602, USA.
Flierl
Michael A
MA
Ward
Peter A
PA
D000818:Animals; D017209:Apoptosis; D001341:Autonomic Nervous System / Q000276:immunology / Q000378:metabolism; D001779:Blood Coagulation Factors / Q000276:immunology / Q000378:metabolism; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D005342:Fibrinolysis; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism*; D009102:Multiple Organ Failure / Q000276:immunology* / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism
D001779:Blood Coagulation Factors; D016207:Cytokines; D018836:Inflammation Mediators; D051193:Toll-Like Receptors; D003165:Complement System Proteins