The endothelium in sepsis: source of and a target for inflammation.
OBJECTIVE
To discuss a possible role of the endothelium in sepsis.


METHODS
Studies published in biomedical journals and our own experimental results.


METHODS
Studies on endothelial mechanisms in the context of sepsis.


METHODS
Changes in endothelial cells on activation by inflammatory stimuli are reviewed briefly; potential mechanisms that lead to endothelial damage during sepsis are discussed.


CONCLUSIONS
The endothelium is a key organ involved in the pathogenesis of sepsis. Dysfunction of or injury to the endothelium may be involved in the pathogenesis of multiple organ failure and should be discriminated from activation resulting from stimulation with inflammatory stimuli. Identification of the molecular mechanisms that contribute to endothelial dysfunction or damage is likely to provide novel targets for the treatment of sepsis.
Hack
C E
CE
Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.
Zeerleder
S
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D000818:Animals; D000925:Anticoagulants / Q000276:immunology; D001777:Blood Coagulation / Q000276:immunology; D003167:Complement Activation / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000276:immunology*; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D009102:Multiple Organ Failure / Q000276:immunology / Q000382:microbiology; D009569:Nitric Oxide / Q000276:immunology; D011486:Protein C / Q000276:immunology; D018805:Sepsis / Q000150:complications / Q000276:immunology*; D018180:Thrombomodulin / Q000276:immunology
D000925:Anticoagulants; D016207:Cytokines; D018836:Inflammation Mediators; D011486:Protein C; D018180:Thrombomodulin; D009569:Nitric Oxide