Bacterial translocation in multiple organ failure: Cause or epiphenomenon still unproven

Abstract

Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.

Bacterial Translocation to the Thoracic Duct in a Setting of Ischemia, Partial Resection and Reperfusion of the Porcine Liver

“…Recently, increased serum IL-6 and IL-8 levels were found immediately after Pringle maneuver-induced hepatic ischemia [24], suggesting that hepatic ischemia alone causes cell damage and consequently, local cytokine production, systemic spill-over of these cytokines and ultimately BT [25]. This notion may explain the finding of culture positive MLNs, lymph and blood samples at the end of the ischemic period in the present study.…”

Significant changes in the serum levels of IL-6, h-HGF, and type IV collagen 7S during the perioperative period of a hepatectomy: Relevance to SIRS

“…The concept of SIRS 1 has become well accepted in recent years, and the state involving proinflammatory cytokines is now recognized as a step prior to the disease progression from postoperative complications or sepsis to MODS. 2,3 Several reports have indicated the importance of proinflammatory cytokines in the serum to the pathophysiology of surgical stress, rejection in organ transplantation, SIRS, and MODS. 2,[8][9][10][11] IL-6 is mainly produced by Kupffer and Ito cells in the hepatic sinusoids, by vascular endothelial cells, and by fibroblasts.…”

The effect of transient intestinal ischemia on inflammatory parameters

“…What specific mechanism or series of events leads to extension of the local inflammatory process remains to be elucidated. It is not yet known whether bacterial translocation or excessive proinflammatory cytokine release and am imbalance between pro-and anti-inflammatory cytokines may cause multiple-organ failure [43]. There is, however, growing evidence that the gut and liverboth origin and target of inflammatory cytokines -fulfill a primary role in a local injury creating a systemic inflammation involving a multiple-organ dysfunction and eventually failure [44].…”