Bacterial translocation in clinical intestinal transplantation

Abstract

Infectious complications and sepsis are associated with high morbidity and mortality in human and experimental small bowel transplantation.1 Enteric microflora is thought to play an important role in the genesis of these infections. The transit of viable bacteria through the intestinal epithelium into the lamina propria, and consequently to the mesenteric lymph nodes, peritoneal cavity, and other previously sterile tissues, is called bacterial translocation (BT). Translocation of microorganisms from the GI tract has been demonstrated in animal and human studies.2,3 Although BT has been suggested to be the mechanism responsible for the high rate of infections occurring after clinical small bowel transplantation (SBTx), data are not available. Bacterial overgrowth, alteration of the mucosal barrier function, consequence of preservation injury or acute rejection (AR), and the use of potent immunosuppression have all been considered responsible for BT in SBTx.4–6 The aim of this study was to evaluate the correlation of BT with these events.