EVALUATION OF BACTERIAL TRANSLOCATION IN THE PATHOGENESIS OF MODS IN SEPSIS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The healthy liver serves as an effective barrier to the passage of bacteria and endotoxin from the GI tract into the systemic circulation. However, in severe liver disease such as cirrhosis, impaired defense mechanisms lead to an increased incidence of bacteremia. Bacteremia is a common complication of cirrhosis, with an estimated incidence of 4.5-8.8%. Bacteremia in cirrhotic subjects is associated with a high mortality. Patients with acute liver failure also have an increased risk of bacteremia. The pathophysiology of bacteremia in this patient population is not entirely clear. Several mechanisms have been postulated including impaired T-cell immunity and abnormal leukocyte chemotaxis. However, the most compelling theory is that depressed hepatic reticuloendothelial system function predisposes these patients to bacteremia. These investigators hypothosize that liver injury is associated with decreased ability to clear bacteria. Further, in the setting of sepsis-induced liver injury, they hypothesize that bacterial translocation will result in secondary bacteremia and increase organ injury.