Tumor necrosis factor in sepsis: mediator of multiple organ failure or essential part of host defense?
Tumor necrosis factor-alpha (TNF) exerts numerous influences which, in association with severe infection, subserve both detrimental as well as beneficial host responses. The current review addresses recent insights into the structure and function of this pleiotropic cytokine, with a particular emphasis upon cellular and organ system consequences of sepsis-induced TNF activity. A comparison of responses elicited by endotoxin or TNF administration are discussed as are mechanisms of endogenous TNF regulation, such as soluble receptors, anti-inflammatory cytokines, and counter-regulatory responses. A review of past and future clinical strategies for altering TNF activity during sepsis is also provided.
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van der Poll
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Lowry
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000627:therapeutic use; D002319:Cardiovascular System / Q000503:physiopathology; D002986:Clinical Trials as Topic; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D004211:Disseminated Intravascular Coagulation / Q000503:physiopathology; D004734:Energy Metabolism; D005786:Gene Expression Regulation; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D007116:Immunization, Passive; D008213:Lymphocyte Activation; D009102:Multiple Organ Failure / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D018805:Sepsis / Q000150:complications / Q000503:physiopathology*; D012772:Shock, Septic / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology / Q000502:physiology*
D000911:Antibodies, Monoclonal; D016207:Cytokines; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha