The intestinal tract contains the body’s largest interface between a person and his or her external environment. The complexity of its function is obvious when thinking that at the same time the intestine must serve two opposite functions; the selective permeability of needed nutrients from the intestinal lumen into the circulation and into the internal milieu in general and, on the other hand, the prevention of the penetration of harmful entities including microorganisms, luminal antigens, and luminal proinflammatory factors. The latter function is known as barrier function [1]. The gut barrier function is comprised by three major lines of defence [2]: 1) The biological barrier, which is made up of normal intestinal flora (gut microbiota) responsible for colonization resistance; 2) The immune barrier, which is composed of gut associated lymphoid tissue (GALT), effector and regulatory T cells, IgA producing B (plasma) cells, group 3 innate lymphoid cells, and, resident macrophages and dendritic cells in the lamina propria; and 3) The mechanical barrier, consisting of the closed-lining intestinal epithelial cells and by the capillary endothelial cells. The epithelial and endothelial cells come into the closest possible contact in the most apical part of the lateral cell membranes (“kissing points”) by specific structures named “tight junctions”(TJs), which interconnect the cells and restrict the passage of ions, molecules and cells through the paracellular space [2, 3]. The term “bacterial translocation”(BT), was first described by Berg and Garlington in 1979, as the phenomenon of passage of viable bacteria from the gastrointestinal tract through the epithelial mucosa into the lamina propria and then to the mesenteric lymph nodes and possibly other normally sterile organs [4]. This initial definition was later widened to include the translocation of non-viable bacteria or their products, namely pathogen-associated molecular patterns (PAMPs), with main representative the intestinal endotoxin. BT occurs in healthy individuals in a low rate of 5-10%, serving two main physiological roles; the antigenic exposure of the gut immune system to be prepared for an effective immune response in case of extensive pathogen invasion, and the development of immune tolerance to several microbial antigens of commensal microflora [5-7]. The intestinal barrier is compromised in several disease states leading to an increased level of BT associated with infectious complications and promotion of a systemic inflammatory response that aggravates the pathophysiological consequences of the underlying disease [8-13]. There are three main pathophysiological groups of intestinal barrier failure associated with pathologic conditions: 1) The intestinal barrier failure observed in surgical patients subjected to major operations for diverse reasons (major liver resections, bowel resections for malignancy, bowel transplantation, aortic aneurysm repair). In this group of patients, increased BT is associated with increased postoperative infectious complications [5, 11, 14-17]. The connecting mechanism is translocation of gut-derived pathogens through a dysfunctional mucosal barrier to the mesenteric lymph nodes, the portal vein and the systemic circulation, eventually leading to postoperative infections [18]. Also, this is the mechanism by which the necrotic pancreas becomes infected in patients with severe necrotic pancreatitis [19]. 2) The second group includes critically ill patients, severely injured or septic, hospitalized in intensive care units. Increased gut permeability is associated with the development of systemic inflammatory response and multiple organ dysfunction syndrome (MODS) in these patients. However, the …